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How do we regulate respiration?

How do we regulate respiration?


School: Florida State University
Department: Physical Education Theory
Course: Functional Anatomy and Physiology I
Professor: Arturo figueroa-galvez
Term: Summer 2016
Cost: 50
Description: FInal exam material
Uploaded: 12/09/2016
28 Pages 290 Views 9 Unlocks

Study Guide for Exam 4

How do we regulate respiration?

The Respiratory System

Mechanics of breathing  

∙ Alveoli: most important part of the lungs because this is where the exchange of gases occur  ∙ Capillary exists on the respiratory membrane and receives venous blood from the right ventricle ∙ Diffusion occurs (remember that the gradient moves from high to low pressure)

∙ The function of the respiratory bronchioles is to facilitate gas exchange -> occurs in the “conducting zone” ∙ To move the O2 from the outside to the inside, we need a pressure gradient -> High in the environment to  Low inside

∙ The action of breathing in and out is due to changes of pressure within the thorax, in comparison with the  outside. This action is also known as external respiration. When we inhale the intercostal muscles (between  the ribs) and diaphragm contract to expand the chest cavity. The diaphragm flattens and moves downwards  and the intercostal muscles move the rib cage upwards and out.

What happens in the lung capillaries is the same thing that happens in the body capillaries?

∙ This increase in size decreases the internal air pressure and so air from the outside (at a now higher pressure  that inside the thorax) rushes into the lungs to equalize the pressures.

∙ When we exhale the diaphragm and intercostal muscles relax and return to their resting positions. This  reduces the size of the thoracic cavity, thereby increasing the pressure and forcing air out of the lungs. ∙ Breathing Rate

∙ The rate at which we inhale and exhale is controlled by the respiratory centre, within the Medulla Oblongata  in the brain. Inspiration occurs due to increased firing of inspiratory nerves and so the increased recruitment  of motor units within the intercostals and diaphragm. Exhalation occurs due to a sudden stop in impulses  along the inspiratory nerves.

In respiratory system, what is alveoli?

If you want to learn more check out Why do banks securitize mortgages?

∙ Our lungs are prevented from excess inspiration due to stretch receptors within the bronchi and bronchioles  which send impulses to the Medulla Oblongata when stimulated.

∙ Breathing rate is all controlled by chemoreceptors within the main arteries which monitor the levels of Oxygen  and Carbon Dioxide within the blood. If oxygen saturation falls, ventilation accelerates to increase the volume  of Oxygen inspired.

∙ If levels of Carbon Dioxide increase a substance known as carbonic acid is released into the blood which causes  Hydrogen ions (H+) to be formed. An increased concentration of H+ in the blood stimulates increased  ventilation rates. This also occurs when lactic acid is released into the blood following high intensity exercise. If you want to learn more check out What is an example of a corporate crime?

Pressure relationships in the thoracic cavity  

∙ Diaphragm allows us to change our thoracic cavity VOLUME -> changes the pressure ->If Lungs INCREASE in  volume = Pressure in the lungs DECREASES = Air moves into the lungs

∙ When the diaphragm relaxes, it moves up -> volume decreases -> pressure increases -> air moves out of the  lungs Don't forget about the age old question of Why is u.s. supreme court performance often difficult to predict?

∙ During contraction, the diaphragm moves down -> increases volume in the thoracic cavity ∙ Abdominals are secondary respiratory muscles

∙ INHALATION -> External Intercostals = E for Elevate the Ribs -> Volume goes up

∙ EXHALATION -> Internal Intercostals  

∙ Most abundant gas in the atmosphere = Nitrogen => .79 * 760mmHg = 600mmHg = Partial Pressure of  Nitrogen

∙ Most important gas in the atmosphere = Oxygen => .21 * 760mmHg = 160mmHg = Partial Pressure of Oxygen

Study Guide for Exam 4

∙ ΔP for CO2 = 5mmHg (45mmHg – 40mmHg)

∙ ΔP for O2 = ~60mmHg (100mmHg – 40mmHg)

∙ Easier for CO2 to diffuse across membranes

o The pressure in the arterial tree will be the same until they reach the systemic capillaries o for CO2, the pressure goes from 45 to 40 when it enters the alveolus and the pulmonary capillary Don't forget about the age old question of What is a proposed benefit of ocean fertilization?

o From pulmonary veins the blood will go the left atrium --> left ventricle --> aorta --> all the branches  until that blood reaches the systemic capillaries...same partial pressures for oxygen and CO2 o the cells have a partial pressure O2 of 40mmHg and partial pressure CO2 of 45mmHg (BLUE) o There is less O2 in the cell than in the blood, therefore the O2 diffuses from the blood to the cells o An equilibrium will always be made

Pulmonary ventilation - Physical factors influencing pulmonary ventilation. Size of  the thoracic cavity(determined by respiratory muscles) and change in pressures in  the lungs.

∙ How do we regulate respiration?

o Medulla oblongata contains the cardiovascular center, and the respiratory centers are also in the  brain stem (some are in the bones) and the medulla oblongata therefore also controls respiration  regularity and depth; inspiratory and expiratory areas inside the medulla We also discuss several other topics like Why don’t we use our nuclear weapons?

o From these areas, there are neurons going to the respiratory muscles- inspiratory muscles  (diaphragm) and expiratory muscle (abdominals) 

∙ The peripheral chemoreceptors are the ones that we need to focus on mainly

o the difference between the central and peripheral chemoreceptors are the nervous systems to which  they belong: central = CNS, peripheral = carotid and aortic arteries

o the receptors respond to chemical substances in blood that are related to respiration- O2, CO2, H+

Study Guide for Exam 4

o Are H+ ions related to CO2 or O2? CO2; excessive CO2 = excessive H+; excessive H+ = excessive  CO2  

o Hypoxia: reduced oxygen; occluding the arteries and inducing exercise can cause the muscles to  become hypoxic and secrete more lactic acid; when a tissue is getting low oxygen due to low oxygen  in the blood, there is an increase in CO2 and therefore an increase in H+ ions, so the most important  receptors are for this situation If you want to learn more check out What is erosion?

o The action potentials then travel to the respiratory centers in the medulla oblongata which innervate  the respiratory muscles, causing us to breathe faster and harder because of the excessive CO2 and H+  ions

∙ Airway resistance is the resistance to flow of air caused by friction with the airways, which includes the  conducting zone for air, such as the trachea, bronchi and bronchioles. The main determinants of airway  resistance are the size of the airway and the properties of the flow of air itself.

∙ The radius of the airways of the conducting zone become smaller as air goes deeper into the lungs. Therefore  the resistance to air in the bronchi is greater than the resistance to air in the trachea. The number of airways  also plays a large role in the resistance to air, with more airways reducing resistance because there are more  paths for the air to flow into. Therefore, despite the fact that the terminal bronchioles are the smallest airway  in terms of radius, their high number compared to the larger airways means that the bronchi actually have  greater resistance because there are less of them compared to the terminal bronchioles. Another important  fact is that airway resistance is inversely related to lung volumes because the airways expand a bit as they  inflate, so the airways in a fully inflated lung will have lower resistance than a lung after exhalation.

Dead space and alveolar ventilation  

∙ dead space is the volume of air which is inhaled that does not take part in the gas exchange, either because it  (1) remains in the conducting airways, or (2) reaches alveoli that are not perfused or poorly perfused. In other  words, not all the air in each breath is available for the exchange of oxygen and carbon dioxide.  Mammals breathe in and out of their lungs, wasting that part of the inspiration which remains in the  conducting airways where no gas exchange can occur.  

∙ Benefits do accrue to a seemingly wasteful design for ventilation that includes dead space.  o Carbon dioxide is retained, making a bicarbonate-buffered blood and interstitium possible. o Inspired air is brought to body temperature, increasing the affinity of hemoglobin for oxygen,  improving O2 uptake.  

o Particulate matter is trapped on the mucus that lines the conducting airways, allowing its removal  by mucociliary transport.

o Inspired air is humidified, improving the quality of airway mucus.

∙ In humans, about a third of every resting breath has no change in O2 and CO2levels. In adults, it is usually in  the range of 150 mL.

∙ Dead space can be increased (and better envisioned) by breathing through a long tube, such as a snorkel. Even  though one end of the snorkel is open to the air, when the wearer breathes in, they inhale a significant  quantity of air that remained in the snorkel from the previous exhalation. Thus, a snorkel increases the  person's dead space by adding even more "airway" that doesn't participate in gas exchange.

Study Guide for Exam 4

Gas exchange between blood, lungs and tissues. Partial pressures of O2 and CO2  in atmospheric air, alveolus, pulmonary circulation, systemic circulation and cells.  

∙ the cells have to diffuse CO2 to the blood, and the hemoglobin is fully saturated (100%) and is dissolved in the  plasma to enter the cells

∙ 10% of the CO2 from the cells is dissolved in the plasma (mainly water with proteins), which is a series of  reactions that produces carbonic acid and hydrogen atoms (see the chart reaction above) ---> first way CO2  travels

∙ then 20% of the CO2 from the cells enters the hemoglobin as one oxygen molecule leaves from the blood in  order to diffuse to the cells; CO2 directly forces one O2 to leave the hemoglobin --> second way CO2 travels ∙ 70% of the CO2 travels in the form of bicarbonate in the plasma after it is produced in the RBC...travels in the  plasma!

o the main form in which CO2 travels in the plasma is bicarbonate

o the secondary form in which CO2 travels in the RBC is attached to the hemoglobin

∙ Oxygen enters into the RBC because it has 3 O2 and 1 CO2, so the CO2 leaves and gives the 1 O2 molecules its  spot in the hemoglobin

o the most important traveling form is via bicarbonate in the plasma...this bicarbonate enters the RBC,  binds to the hydrogen from the hemoglobin, which makes carbonic acid, in which the CO2 diffuses  into the alveolus/ blood

o the most important part is how the new oxygen will force the release of CO2 from the hemoglobin o the movement of bicarbonate from the plasma into the RBC

o what happens in the systemic capillary is called Bohr and what happens in the respiratory capillary is  called the systemic effect

∙ As the external intercostals & diaphragm contract, the lungs expand. The expansion of the lungs causes the  pressure in the lungs (and alveoli) to become slightly negative relative to atmospheric pressure. As a result, air  moves from an area of higher pressure (the air) to an area of lower pressure (our lungs & alveoli). During  expiration, the respiration muscles relax & lung volume decreases. This causes pressure in the lungs (and  alveoli) to become slight positive relative to atmospheric pressure. As a result, air leaves the lungs.

∙ Partial Pressure: the individual pressure exerted independently by a particular gas within a mixture of gasses.  The air we breathe is a mixture of gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow  into a balloon creates pressure that causes the balloon to expand (& this pressure is generated as all the  molecules of nitrogen, oxygen, & carbon dioxide move about & collide with the walls of the balloon).  However, the total pressure generated by the air is due in part to nitrogen, in part to oxygen, & in part to  carbon dioxide. That part of the total pressure generated by oxygen is the 'partial pressure' of oxygen, while  that generated by carbon dioxide is the 'partial pressure' of carbon dioxide. A gas's partial pressure, therefore,  is a measure of how much of that gas is present (e.g., in the blood or alveoli).

∙ the partial pressure exerted by each gas in a mixture equals the total pressure times the fractional  composition of the gas in the mixture. So, given that total atmospheric pressure (at sea level) is about 760 mm  Hg and, further, that air is about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times 760  mm Hg or 160 mm Hg.

∙ Partial Pressures of O2 and CO2in the body (normal, resting conditions):  

(http://highered.mheducation.com/sites/0072495855/student_view0/chapter25/animation__gas_exchange_during_respiration.html) o Alveoli

▪ PO2 = 100 mm Hg

Study Guide for Exam 4

▪ PCO2 = 40 mm Hg

o Alveolar capillaries

▪ Entering the alveolar capillaries

▪ PO2 = 40 mm Hg (relatively low because this blood has just returned from the systemic  circulation & has lost much of its oxygen)

▪ PCO2 = 45 mm Hg (relatively high because the blood returning from the systemic circulation  has picked up carbon dioxide)

Study Guide for Exam 4

∙ While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from the alveoli into the blood  & carbon dioxide from the blood into the alveoli.

o Leaving the alveolar capillaries

▪ PO2 = 100 mm Hg

▪ PCO2 = 40 mm Hg

∙ Blood leaving the alveolar capillaries returns to the left atrium & is pumped by the left ventricle into the  systemic circulation. This blood travels through arteries & arterioles and into the systemic, or body, capillaries.  As blood travels through arteries & arterioles, no gas exchange occurs.

o Entering the systemic capillaries

▪ PO2 = 100 mm Hg

▪ PCO2 = 40 mm Hg

o Body cells (resting conditions)

▪ PO2 = 40 mm Hg

▪ PCO2 = 45 mm Hg

∙ Because of the differences in partial pressures of oxygen & carbon dioxide in the systemic capillaries & the  body cells, oxygen diffuses from the blood & into the cells, while carbon dioxide diffuses from the cells into  the blood.

o Leaving the systemic capillaries

▪ PO2 = 40 mm Hg

▪ PCO2 = 45 mm Hg

∙ Blood leaving the systemic capillaries returns to the heart (right atrium) via venules & veins (and no gas  exchange occurs while blood is in venules & veins). This blood is then pumped to the lungs (and the alveolar  capillaries) by the right ventricle.

External respiration: partial pressure gradients  

• What happens in the lung capillaries is the same thing that happens in the body capillaries

Study Guide for Exam 4

∙ First, "blue blood" (75% saturation O2) comes from the right ventricle (branch of pulmonary artery), and the  venous side of the tissue capillaries ---> rich in CO2, low O2 ---> must go to lungs to be oxygenated ∙ This is a process of simple diffusion because they are gases

∙ in the alveolus there is a constant partial pressure O2 =100; to have diffusion, there must be a difference in  two places (of pressure)

∙ the blood has 40mmHg O2, and the alveolus always has 100mmHg = difference of 60mmHg ---> a lot of oxygen  will diffuse because there is a great difference

∙ the blood has 60mmHg ---> smaller diffusion amount; pressure of O2 increases

∙ the blood has 80mmHg ---> even less O2 diffusion from alveolus to the blood

∙ the blood has 100mmHg ---> no more diffusion because there is an equilibrium

∙ this is why the lung capillaries have the same amount of O2; because there is the same pressure ∙ CO2 is the same thing: alveolus has 40mmHg CO2

∙ when the blood enters with 45mmHg Co2, blood diffuses from blood to alveolus, causing a lower diffusion of  40mmHg until equilibrium is reached

∙ alveolus maintains same pressures because we continue to breathe; if we stopped breathing, then we would  also stop diffusing CO2 and O2 from blood to alveolus

Transport of respiratory gases by blood (Oxy-Hb dissociation curve)

∙ Saturated hemoglobin- when all four hemes of the molecule are bound to O2 = 100% o hemoglobin is a protein in the RBC and its function is to transport oxygen, among other things o in the oxygenated blood, each hemoglobin molecule has 4 places for oxygen; when 4 molecules bind  

to HB, it is 100% saturated (it's actually 98% because it supplies some to the tissue in the lungs, but  just know it is basically 100% for the purposes of this class)

o what is the pressure produced by 20mL of O2? 100mmHg

▪ Oxy-Hemoglobin Saturation curve

Study Guide for Exam 4

▪ 100mmHg partial pressure in the RED of the other figure, which is at the top of the curve, is  20mL volume O2 unloaded to the tissues, and also 100% saturation  

▪ partial pressure for the cells (PURPLE) is 40mmHg, so a lot of oxygen diffuses from the blood  to the cells, which causes the pressure to decrease to this value

∙ why 40? because that is the pressure in the cell and this makes everything fall into  equilibrium

▪ here at 40mmHg, there is 75% saturation (one molecule O2 leaves from each hemoglobin) of  O2 and 15 mL O2...we are diffusing O2 from the blood to the cells, and the volume is  

decreasing causing a decrease in pressure

o At the beginning (arteries), the volume is 20mL and at the end (veins) it is 15mL...arterial venous  oxygen difference is 5mL O2 (this goes to the cells)

▪ When exercising, the muscles use more of the O2 so the pressure will drop...say to 20mmHg,  making the volume of oxygen decrease in the venous blood and a lower saturation

∙ The part of the curve you should know is the top part- this is the level of the systemic capillary from the  arterial blood to the venous blood

∙ the arterial blood has a partial pressure of O2 of 100mmHg from 20mL O2, which means the hemoglobin is  100% saturated

∙ if this blood enters the systemic capillary (more O2 than the cells) ---> diffusion; arterial blood looses O2  (graph line moves down)

∙ if we lose volume, we lose pressure; if we lose pressure, the hemoglobin is losing saturation; at the end of  capillary, 40mmHg from 15mL O2, saturation of hemoglobin is 75%

∙ Transport of Co2

o Co2 produced by the cells from anaerobic metabolism in the body (lactic acid) enters the capillary: ▪ 10% ---> mix with water, produce carbonic acid, dissociates to carbon and hydrogen ions in  the plasma

▪ 20% ---> combines with hemoglobin (1 molecule has 4 places for O2); systemic capillary combines with hemoglobin so it pushes an oxygen from hemoglobin and saturation is now  75%

▪ 70% ---> CO2 combines with water, produces carbonic acid, dissociates into bicarbonate with  goes out into the plasma; MAIN WAY is to transform into bicarbonate, which will be in the  plasma

▪ How can we get rid of excessive H+ ions? Not through respiration... convert and combine  with bicarbonate to change to CO2 to eliminate

▪ This also happens in the kidneys; the kidneys and the lungs work together to reach  homeostasis for the ions and CO2; depending on the situation- running really hard and fast  causes excessive release of CO2 from the lungs, not the kidneys; if someone with a  

pulmonary disease, the kidneys must help out and excess H+ ions are eliminated via urine Control of respiration. Role of peripheral and central chemoreceptors

∙ Focus on chemoreceptors- peripheral and central (slide#46, respiratory)

o peripheral chemoreceptors are in the large arteries; stimulated by a decrease in O2, increase in CO2, and an increase in H+ (DIRECT/ strongest is high CO2!)

▪ CO2 directly stimulates the peripheral chemoreceptors

o What is the direct stimulus to the central chemoreceptors?

Study Guide for Exam 4

▪ The CNS (brain and spinal cord) are surrounded by cerebrospinal fluid (water)

▪ Not many substances are allowed to cross the blood brain barrier (contains cerebrospinal  fluid)

▪ CO2 diffuses very easily (NOT H+ ions) out of the blood to the CF (water) to make  carbonic acid, which dissociates to H+ ions and bicarbonate

▪ H+ ions DIRECTLY stimulate the central chemoreceptors; CO2 INDIRECTLY stimulates the  central chemoreceptors

∙ Chemoreceptor regulation of breathing is a form of negative feedback. The goal of this system is to keep  the pH of the blood stream within normal neutral ranges, around 7.35.

∙ A chemoreceptor is a sensory receptor that transduces a chemical signal into an action potential. The  action potential is sent along nerve pathways to parts of the brain, which are the integrating centers for  this type of feedback. There are many types of chemoreceptors in the body, but only a few of them are  involved in respiration.

∙ The respiratory chemoreceptors work by sensing the pH of their environment through the concentration  of hydrogen ions. Because most carbon dioxide is converted to carbonic acid (and bicarbonate) in the  bloodstream, chemoreceptors are able to use blood pH as a way to measure the carbon dioxide levels of  the bloodstream.

∙ The main chemoreceptors involved in respiratory feedback are:

o Central chemoreceptors: These are located on the ventrolateral surface of medulla oblongata and  detect changes in the pH of spinal fluid. They can be desensitized over time from chronic hypoxia  (oxygen deficiency) and increased carbon dioxide.

o Peripheral chemoreceptors: These include the aortic body, which detects changes in blood  oxygen and carbon dioxide, but not pH, and the carotid body which detects all three. They do not  desensitize, and have less of an impact on the respiratory rate compared to the central  chemoreceptors.

∙ Chemoreceptor Negative Feedback

o Negative feedback responses have three main components: the sensor, the integrating sensor,  and the effector. For the respiratory rate, the chemoreceptors are the sensors for blood pH, the  medulla and pons form the integrating center, and the respiratory muscles are the effector.

o Consider a case in which a person is hyperventilating from an anxiety attack. Their increased  ventilation rate will remove too much carbon dioxide from their body. Without that carbon  dioxide, there will be less carbonic acid in blood, so the concentration of hydrogen ions decreases  and the pH of the blood rises, causing alkalosis.

o In response, the chemoreceptors detect this change, and send a signal to the medulla, which  signals the respiratory muscles to decrease the ventilation rate so carbon dioxide levels and pH  can return to normal levels.

∙ There are several other examples in which chemoreceptor feedback applies. A person with severe diarrhea  loses a lot of bicarbonate in the intestinal tract, which decreases bicarbonate levels in the plasma. As  bicarbonate levels decrease while hydrogen ion concentrations stays the same, blood pH will decrease (as  bicarbonate is a buffer) and become more acidic.

o In cases of acidosis, feedback will increase ventilation to remove more carbon dioxide to reduce  the hydrogen ion concentration. Conversely, vomiting removes hydrogen ions from the body (as  the stomach contents are acidic), which will cause decreased ventilation to correct alkalosis.

Study Guide for Exam 4

o Chemoreceptor feedback also adjusts for oxygen levels to prevent hypoxia, though only  the peripheral chemoreceptors sense oxygen levels. In cases where oxygen intake is too low,  feedback increases ventilation to increase oxygen intake.

The Urinary System


Nephrones: capillary beds, peritubular capillaries, the JG apparatus  

∙ Nephron = functional unit of the kidneys

o two components: (1) vascular and (2) tubular)

o blood flows from the renal artery to the afferent arteriole (Afferent...A = first, toward) to the  glomerulus, then to the second arteriole, the Efferent arteriole (Efferent...away from) then to the  peritubular capillaries, then to the veins where it is drained

Study Guide for Exam 4

o the bowman's capsule continues with a segment connected to the proximal convoluted tubule, then  to the loop of Henle, then to the distal convoluted tubule, and finally to the collecting ducts that drain  urine to the kidney's pelvis

∙ Cortical nephrons are in the cortex, and the other ones are juxtamedullary nephrons- a little deeper in the  cortex, and their loop of Henle are in the medulla

∙ 85% of neurons are in the cortex and produce regular urine, and juxtamedullary make different urine ∙ because they are tubes, they are covered with epithelial cells

o the proximal convoluted tubule has a lot of mitochondria

o the distal convoluted tubule has less mitochondria

o the loop of Henle and the collecting duct cells don't have many at all

o therefore the proximal is more active and is the primary site for reabsorption

∙ the afferent arteriole controls blood flow

∙ juxtaglomerular cells are the smooth muscle cells in the afferent arteriole

o form an enzyme called Renin  

o the cells in the proximal convoluted tubules communicate with the juxtaglomerular cells which  communicate with the arterioles to control filtration (the formation of urine)

∙ the Bowman's capsule has epithelial cells also

∙ Nephrons

o Functional unit of the kidney; tubule system that filters out wastes and other unnecessary chemicals  circulating in the blood

o "filtering" is the result of tubule cell's ability to change its permeability

o 85% of nephrons are cortical; 15% are juxtamedullary

o glomerular (Bowman's) capsule

o Note: the glomerular capsule + the glomerulus = renal corpuscle

o proximal convoluted tubule (PCT)

o loop of Henle (ascending and descending limb)

o distal convoluted tubule (DCT)

o collecting tubule - papillary duct - calyces

o Capillary beds (microvasculature) of nephron are composed of two capillary  

beds, glomerular (feeding nephron) and peritubular (surrounding nephron)

o Glomerulus is fed and drained by arterioles (afferent and efferent) which arise from interlobular  arteries that run through the renal cortex; due to arterioles being high-resistance vessels and afferent  arterioles having larger diameters than efferent, blood pressure is high, therefore fluid and solute are  forced out of blood into the glomerular capsule; most filtrate is returned to blood via peritubular  capillary bed surrounding the nephron.

∙ Juxtaglomerular Apparatus

o Region where the coiling distal tubule lies against the afferent arteriole feeding the glomerulus o Both arteriole and distal tubule has specialized cells:

o juxtaglomerular cells (JG) - smooth muscle cells surrounding the afferent and efferent artioles and  composed of granules containing renin; these cells act as mechanoreceptors that sense the blood  pressure in the arteriole

o macula densa - distal tubule cells that act as chemoreceptors or osmoreceptors that respond to  changes in solute concentration of filtrate in distal tubule

o Therefore, both aid in the regulation systemic blood pressure and rate of filtration formation!

Study Guide for Exam 4

Regulation of glomerular filtration, extrinsic controls: neural and hormonal  

∙ Glomerulus filtration: filtration in the glomerulus; controlled by 3 mechanisms

o sympathetic activity decreases ---> basal dilation ---> more blood flow to the glomerulus ---> more  blood volume ---> more pressure ---> more filtration ---> urine formation increases (as when resting) o sympathetic activity increases ---> basal constriction --> less blood flow to the glomerulus ---> less  blood volume ---> pressure decreases ---> less filtration ---> urine formation decreases (as when  exercising)

o Hormonal regulation: ADH and aldosterone (previous lectures)

∙ the renal artery enters into the afferent arteriole and continues into the kidney for filtration; some substances  will not filter in the glomerulus but rather in the distal convoluted tubule from the peritubular cavity; after all  the collecting ducts, the tubes will drain into the ureter

∙ The end of the ureter enters into the urinary bladder, which is mostly smooth muscle, the most important of  which is called the detrusor muscle

∙ homeostatic regulation- equilibrium is trying to be maintained through these processes; we need water to  produce BP...if BP is low, we need water to increase blood volume and therefore BP

o short term = ANS

o long term = kidneys; BP and pH

∙ Regulation of glomerular filtration (influence on blood pressure)

o renal autoregulation (myogenic mechanism and JG apparatus)

▪ Myogenic control of afferent arteriole

∙ Increase in BP and increase in GFR causes a loss of nutrients which stimulate  

myogenic cells constrict afferent arteriole

∙ Decrease in BP and decrease in GFR causes waste accumulates which signal  

myogenic cells to relax and cause the afferent arteriole to dilate

▪ JG Apparatus

∙ Juxta-glomerular cell regulation (mechanoreceptors that detect vessel stretch)

o Decrease in BP and decrease in GFR causes a release in rennin

o Renin-Angiotensin mechanism (sodium retention) increases BP and GFR

∙ Macula densa cell regulation (osmoreceptors that sense sodium concentration)

o Increase in BP and increase in GFR causes loss of sodium

o GFR is too high will stimulate macula densa cells to release a vasopressor  

to cause afferent constriction as well as JG cell inhibition

o neural controls (sympathetic nervous system can cause afferent arteriole constriction, deliver less  blood into glomerulus and decrease GFR) Diagram

o hormonal - renin-angiotensin mechanism and antidiuretic hormone

Tubular reabsorption and secretion . Exchange mechanisms: Na-K, H-HCO3

∙ The filtrate contains water and small solutes, such as ions, amino acids, glucose (in a normal, non-diabetic  individual); glucose will not continue into the urine through, because it is reabsorbed into the bloodstream o proteins and RBC are not filtrate!

∙ filtrate moving water and small substances to the glomulus into the proximal convoluted tubule, leaves the  tubule after crossing the epithelial cells and into the peritubular capillary

Study Guide for Exam 4

∙ most of the substances, if we need them will continue to the lumen and make it to the proximal convoluted  tubule where most reabsorption occurs and the distal convoluted tubule is where most of the secretion occurs o primary reabsorption is the in proximal convoluted tubule

o secondary reabsorption is distal convoluted tubule

o primary site for secretion is distal convoluted tubule

∙ the capsule always has fluid and therefore also always has pressure; to move substances there must be a  difference in pressure (high ---> low)

o the pressure in the capsule must be lower than the pressure in the glomerulus

o what produces these pressures in the glomerulus? the volume of blood

o what controls the volume of blood in the glomerulus? the afferent arteriole

o what controls the contraction of the smooth muscles of the afferent arteriole? ANS o is the parasympathetic involved? no

o know the difference between protein and amino acids- a large PRO = several AA vs. a single AA

∙ Tubular reabsorption - hormonally controlled transepithelium process in proximal tubules where water,  nutrients, and ions are reclaimed

∙ Two processes

o Active tubular reabsorption - diffusion by ATP-dependent carrier; transport of glucose, amino acids,  and vitamins

▪ there is cotransportation of molecules

▪ molecules being carried depends upon another molecule's (e.g. Na) transport across  basolateral membrane

o Passive tubular reabsorption - diffusion, facilitated diffusion, and osmosis; substance moves along  electrochemical gradients without the use of energy

▪ sodium movement establishes osmotic gradient

▪ water moves by osmosis into peritubular capillaries

▪ causes obligatory water reabsorption

∙ Nonreabsorbed substances due to:

o a lack of carriers

o not lipid soluble

o too large to pass through plasma membrane pores of tubular cells

o examples: urea, creatine, and uric acid

∙ Reabsorption by region:


▪ 65% sodium ions and water

▪ 100% glucose, lactate, amino acids, vitamin

▪ 90% bicarbonate ions

▪ 50% chloride ions

▪ 55% potassium ions

▪ calcium, phosphate, and magnesium ion (hormonally controlled)

o Loop of Henle

▪ 25% sodium ions

▪ 10% water

▪ 35% chloride

▪ 30% potassium

o DCT (NOTE: not all that remains in DCT will be reabsorbed - review ADH, Aldosterone, and ANP) ▪ 10% sodium ions

▪ 10% chloride ions

▪ 25 % water

Study Guide for Exam 4

Renin-angiotensin-aldosterone system  

∙ The Renin Angiotensin Aldosterone System

o what is the stimulus for this mechanism? low BP (dehydration, bleeding, sweating, etc.) o renin from the wall of the afferent arteriole into the blood

o finds its substrate, angiotensinogen (PRO produced by liver)

o renin cuts a piece of those amino acids called angiotensin 1 (10 amino acids) is inactive o when angiotensin 1 arrives at the pulmonary capillaries, ACE (angiotensin converting enzyme)  converts 1 to angiotensin 2 but cutting amino acids (now 8 amino acids)

o angiotensin 2 goes to the smooth muscles of the arteries to cause vasoconstriction and also goes to  the adrenal gland cortex to promote the secretion of aldosterone

o aldosterone goes to the kidney tubules and promotes the exchange between Na+ and K+ o Na+ moves from the lumen of the tubule to the ...reabsorption and K+ is secreted

o Na+ is reabsorbed and water will follow the solute

o water will go to the peritubular capillaries and the BP will increase and K+ is getting out of the body o another stimulus for this system is low Na+ in blood and high K+ in blood (because aldosterone not  only increases BP, it reabsorbs Na+ and secretes K+)

∙ Excess H+ in the blood due to excessive CO2 (breathing really hard) causes the CO2 to be converted to  carbonic acid and H+ ions, which need to be eliminated

o we will reabsorb bicarbonate and secrete the H+ ions

∙ The renin-angiotensin-aldosterone system (RAAS) plays an important role in regulating blood  volume and systemic vascular resistance, which together influence cardiac output and arterial pressure. As the  name implies, there are three important components to this system: 1) renin, 2) angiotensin, and 3)  aldosterone. Renin, which is released primarily by the kidneys, stimulates the formation of angiotensin in  blood and tissues, which in turn stimulates the release of aldosterone from the adrenal cortex.

∙ Renin is a proteolytic enzyme that is released into the circulation by the kidneys. Its release is stimulated by: ∙ sympathetic nerve activation (acting through β1-adrenoceptors)

∙ renal artery hypotension (caused by systemic hypotension or renal artery stenosis) ∙ decreased sodium delivery to the distal tubules of the kidney.

∙ Juxtaglomerular (JG) cells

o associated with the afferent arteriole entering the renal glomerulus are the primary site of renin  storage and release. A reduction in afferent arteriole pressure causes the release of renin from the JG

Study Guide for Exam 4

cells, whereas increased pressure inhibits renin release. Beta1-adrenoceptors located on the JG cells  respond to sympathetic nerve stimulation by releasing renin. Specialized cells (macula densa) of  distal tubules lie adjacent to the JG cells of the afferent arteriole. The macula densa senses the  concentration of sodium and chloride ions in the tubular fluid. When NaCl is elevated in the tubular  fluid, renin release is inhibited. In contrast, a reduction in tubular NaCl stimulates renin release by the  JG cells. There is evidence that prostaglandins (PGE2 and PGI2) stimulate renin release in response to  reduced NaCl transport across the macula densa. When afferent arteriole pressure is reduced,  glomerular filtration decreases, and this reduces NaCl in the distal tubule. This serves as an important  mechanism contributing to the release of renin when there is afferent arteriole hypotension, which  can be caused by systemic hypotension or narrowing (stenosis) of the renal artery that supplies blood  flow to the kidney.

∙ When renin is released into the blood, it acts upon a circulating substrate, angiotensinogen, that undergoes  proteolytic cleavage to form the decapeptide angiotensin I. Vascular endothelium, particularly in the lungs,  has an enzyme, angiotensin converting enzyme (ACE), that cleaves off two amino acids to form the  octapeptide, angiotensin II (AII), although many other tissues in the body (heart, brain, vascular) also can form  AII.

∙ AII has several very important functions:

o Constricts resistance vessels (via AII [AT1] receptors) thereby increasing systemic vascular  resistance and arterial pressure

o Stimulates sodium transport (reabsorption) at several renal tubular sites, thereby increasing sodium  and water retention by the body

o Acts on the adrenal cortex to release aldosterone, which in turn acts on the kidneys to increase  sodium and fluid retention

o Stimulates the release of vasopressin (antidiuretic hormone, ADH) from the posterior pituitary, which  increases fluid retention by the kidneys

o Stimulates thirst centers within the brain

o Facilitates norepinephrine release from sympathetic nerve endings and inhibits norepinephrine re uptake by nerve endings, thereby enhancing sympathetic adrenergic function

o Stimulates cardiac hypertrophy and vascular hypertrophy

∙ The renin-angiotensin-aldosterone pathway is not only regulated by the mechanisms that stimulate renin  release, but it is also modulated by natriuretic peptides released by the heart. These natriuretic peptides acts  as an important counter-regulatory system.

∙ Therapeutic manipulation of this pathway is very important in treating hypertension and heart failure. ACE  inhibitors, AII receptor blockers and aldosterone receptor blockers, for example, are used to decrease arterial  pressure, ventricular afterload, blood volume and hence ventricular preload, as well as inhibit and reverse  cardiac and vascular hypertrophy.

ADH effect  

∙ Antidiuretic hormone (ADH) is produced by the pituitary gland to control the amount of water that is  reabsorbed through the collecting ducts

∙ ADH helps aldosterone (they are synergists)

o what produces ADH? hypothalamus

o where is ADH secreted? posterior pituitary

Study Guide for Exam 4

o Anti Diuretic Hormone : hormone that goes against urine secretion; water is reabsorbed and urine is  reduced

o ADH is also in the blood vessels but is called Vasopressin there because it causes smooth muscle  contraction (increases BP)

o reabsorption of water by the effect of ADH is through the formation of aquaporins ∙ An anti-diruetic is a substance that decreases urine volume, and ADH is the primary example of it within the  body. ADH is a hormone secreted from the posterior pituitary gland in response to increased plasma  osmolarity (i.e., increased ion concentration in the blood), which is generally due to an increased  concentration of ions relative to the volume of plasma, or decreased plasma volume.

∙ The increased plasma osmolarity is sensed by osmoreceptors in the hypothalamus, which will stimulate the  posterior pituitary gland to release ADH. ADH will then act on the nephrons of the kidneys to cause a decrease  in plasma osmolarity and an increase in urine osmolarity.

∙ ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are  normally impermeable to water. This effect causes increased water reabsorption and retention and decreases  the volume of urine produced relative to its ion content.

∙ After ADH acts on the nephron to decrease plasma osmolarity (and leads to increased blood volume) and  increase urine osmolarity, the osmoreceptors in the hypothalamus will inactivate, and ADH secretion will end.  Due to this response, ADH secretion is considered to be a form of negative feedback.

Formation of concentrated urine  

∙ when will we form diluted urine? when we are very well hydrated or have hypertension; low solutes, high  water

∙ how do you explain how alcohol causes more frequent urination? because it inhibits ADH and aldosterone  (since they work together)

∙ concentrated urine is just the opposite- high solutes, low water

∙ A diuretic is any substance that has the opposite effect of ADH— they increase urine volume, decrease urine  osmolarity, lead to an increased plasma osmolarity, and often reduced blood volume. Many substances can  act as diuretics, albeit with different mechanisms.

∙ A common example is alcohol and water ingestion, which directly inhibit ADH secretion in the pituitary gland.  Alternatively caffeine is a diuretic because it interferes with sodium reabsorption (reducing the amount of  water reabsorbed by sodium cotransport) and increases the glomerular filtration rate by temporarily  increasing blood pressure. Many medications are diuretics because they inhibit the ATPase pumps, thus  slowing water reabsorption further.

Autonomic control of urination  

∙ Relaxed smooth muscle and contracted sphincter = no urination (bladder is not full, 200-300 ml urine volume  and the parasympathetic activity decreases, causing inhibition)

∙ Contracted smooth muscle and relaxed sphincter = urination (bladder reaches 500-600 ml urine volume and  the parasympathetic activity increases, causing stimulation)

o We still control urination by sending signals down to the spinal cord and control the skeletal muscle  until we can't control it anymore (fatigue), causing us to urinate

∙ The nerves that control your bladder can be described as follows:

Study Guide for Exam 4

∙ Parasympathetic nerves from the S2, S3 and S4 levels of your spinal cord cause the upper part of your bladder  to contract and your bladder neck to relax, assisting in the process of micturition (urination). ∙ Sympathetic nerves from the T11-L2 levels of your spinal cord do the opposite, causing the upper section of  the bladder to relax and the bladder neck to contract, ensuring you can store urine.

∙ Internal urethral sphincter nerves

o The nerves that control your urethral sphincter can be described as follows:

o Parasympathetic nerves from the S2, S3 and S4 levels of the spinal cord control the internal sphincter,  causing it to relax to allow urine to pass out of the bladder.

o Sympathetic nerves from the T11-L2 levels of the spinal cord cause the internal urethral sphincter to  tighten, helping to hold stored urine in the bladder.

o Both of these functions are involuntary. This means that they operate in an automatic or reflex way,  beyond your control.

∙ External urethral sphincter nerves

o Nerves from the S2-S4 levels of your spinal cord control your external urethral sphincter. This  sphincter is able to be voluntarily or consciously controlled.

∙ Filling and emptying your bladder

o When the amount of urine in your bladder reaches around 250ml, sensors in your bladder muscle are  stimulated. Your bladder signals your brain, and you will feel a slight urge to pass urine. Once you  have around 400-500 ml in your bladder, this urge grows in intensity and you need to empty your  bladder.

o When full, the stretch receptors in your bladder stimulate nerves to initiate the  

subconscious reflex called the micturition reflex. The final stage of urination remains in your  conscious control, until you can access an appropriate place and relax the external sphincter.

The Digestive System

Basic functional concepts and understand the basic structure of the GI tract  

∙ We must absorb the nutrients we consume in their simplest form; we eat carbohydrates in complex forms but  we don't absorb them in this manner- this is why we need digestive enzymes that are produced by glands ∙ How many groups of glands do we have?  

o endocrine (secrete into the bloodstream) and exocrine (secrete to the lumen of the gastrointestinal  tubes)

∙ Accessory enzymes: salivary glands (salivary amylase), gallbladder (bile- not en enzyme but aids in digestion),  liver (stores bile), and pancreas (insulin, etc.)

∙ Stomach: starts the digestion of PRO, continues digestion of CHO (begins in the mouth with salivary amylase),  moves the chyme to the small intestine

∙ Small intestine: Duodenum (most important because it receives secretions from the liver and pancreas; main  place of digestion), Jejunum (absorbs the nutrients), and Ileum (transports the nutrients) o Epithelial cells: one layer in the stomach and intestines; not more because it would be more difficult  to move substances back into the blood

o Duct: from exocrine glands that secrete mucous or enzymes; production drains to the lumen o Mucosa and submucosa are separated by a thin layer of smooth muscle that isn't vital to the function ▪ mucosa- main role is to produce mucous which protects the wall; if we didn't have it we  would be in pain; contains blood vessels

Study Guide for Exam 4

▪ muscle: most external layer of the mucosa is longitudinal smooth muscle; most internal layer  is circular smooth muscle; if the smooth muscle follows the circumference of the tube, it is  circular; if the smooth muscle follows the length of the tube, it is longitudinal; circular layer  decreases the diameter while the longitudinal layer pushes the content down the tube

▪ the nerves in the mucosa provide the neurotransmitters to stimulate smooth muscle  contraction and action potentials for the glands to secrete; the nerves are controlled by the  ANS...function of the gastrointestinal system is movement of substances in the lumen, so  they need to contract the smooth muscle and stimulate secretion of the glands (mucous and  enzymes), so the parasympathetic is the stimulator and the sympathetic is the inhibitor ∙ myenteric nerve plexus- muscle

∙ submucosal nerve plexus- enzymes and mucous

∙ There are two ways to break down food- mechanical and chemical

o first place of mechanical is with the teeth in the mouth

o chemical digestion is produced by the enzymes:

▪ mouth: salivary enzymes (CHO)

▪ stomach: enzymes for PRO

▪ small intestine: duodenum- pancreatic enzymes and bile (fat emulsification)

▪ lymph vessels: absorb the simple nutrients (glucose, amino acids, lipids, etc.)

▪ large intestine: chyme moves here and water and other small nutrients are extracted, then  turned to feces to be defecated in the anal canal and rectum

Gastric secretion, production of the different cells in the gastric glands

∙ Secretion of the exocrine glands is one of the functions and the other function is motility; they will increase or  decrease at the same time (if you are salivating, that means the gastrointestinal glands are also secreting, and  motility is also being promoted; you cannot separate the functions)

o The activation comes from the ANS- increase parasympathetic, decrease sympathetic (opposite increase sympathetic, decrease parasympathetic = reduced gastrointestinal activity)

o What is the difference between the stomach and other glands in the gastrointestinal system? The  layers of muscle- stomach has 3, everything else has only 2

o If the exocrine glands in the mouth are secreting, then the exocrine glands in the stomach also  secrete and motility increases

o the mucosa and the glands are epithelial cells

▪ regular - mucous neck cells produce mucous

▪ specialized- parietal cells and chief cells; produce hormones that go to the blood

∙ parietal secrete HCl (transforms pepsinogen (PRO) to pepsin by cutting amino acids;  first enzyme that begins PRO digestion) and intrinsic factor (body produces it; binds  

to B12 (extrinsic factor) to protect and transport it to the small intestine for  


∙ chief cells secrete pepsinogen

▪ enteroendocrine cells secrete gastrin and CKK

∙ G cells secreted by antrum (part of the stomach) produce gastrin

∙ what stimulates the glands for secretion to the blood? parasympathetic activity  


Study Guide for Exam 4

∙ in the blood, gastrin goes to all the other cells in the gastric wall which then  

stimulates secretion of pepsinogen and HCl to start the digestion of PRO

∙ chief cells and parietal cells are stimulated by gastrin

∙ understand how gastrin is stimulated for secretion

Regulation of gastric secretion. The 3 phases: cephalic, gastric and intestinal  (enterogastric reflex)

∙ Salivation starts because the brain detects something that you like! This is the first phase of  secretion/digestion: cephalic phase - in the head

o impulses sent from the brain in the ANS (medulla oblongata); cortex senses the coffee by the smell  and the image, which communicates with the medulla oblongata, which increases parasympathetic  stimulation, which increases gastrointestinal activity (salivation, secretions, motility)

∙ the first phase is cephalic- the food isn't even in our body yet! Starts in the cortex, goes to the vagus nerve in  the medulla oblongata

o salivation and stomach secretes at the same time

o parasympathetic nervous system is stimulated generally and the whole gastrointestinal system is  stimulated

o food in our mouth is still considered cephalic because it's not in our stomach yet

∙ the second phase is called the gastric phase

o when you move the chyme, the pyloric sphincter is opened and the chyme moves into the duodenum ∙ the third phase is called the intestinal phase because the chyme is in the duodenum ∙ when we have the cephalic phase, the function is to stimulate gastrointestinal function (secretions and  motility)

∙ when we have the gastric phase, the function is to stimulate gastrointestinal function (secretions and motility)  also because we are moving

∙ when we have the intestinal phase, the function is to inhibit the gastrointestinal function (secretions and  motility); the other name is enterogastric reflex

o when we allow small amounts of chyme into the duodenum, it has time to buffer the soution o there are two primary hormones secreted by the epithelial cells in the duodenum: CKK and secretin  (inhibit gastric emptying)

▪ acid in chyme and lipid presence stimulate these hormones

▪ can you separate secretion from motility? no; so if they are decreasing secretion, they are  also decreasing motility and therefore gastrointestinal function and activity

▪ the duodenum must control the acidity of the chyme and the presence of fats- how? ∙ the 2 hormones (CKK and secretin); one goes to the gallbladder to secrete bile and  the other goes to the pancreas

o one is supposed to produce movement in the gallbladder- CKK (kineme =  


o secretin goes to the pancreas to promote secretion

∙ it is connected with the pancreas, liver, and gallbladder

∙ bile helps with the fats, and pancreatic juice (lots of bicarbonate) buffers acidity

∙ bile is produced in the liver from cholesterol (not a bad thing!)

∙ bicarbonate will buffer the pH of the acids and is secreted from the pancreas

Study Guide for Exam 4

∙ pancreas secretes inactive enzymes...if they are active then they would digest the  


o Amylase- digestion of CHO- is also in the pancreas and is inactive until it  

reaches the duodenum

o lipases and proteolitic enzymes also

o and a lot of bicarbonate

o this is pancreatic juice

o once the enzymes reach the duodenum...trypsinogen (inactive) transferred  

to trypsin (active)

∙ The cephalic phase is the stage in which the stomach responds to the mere sight, smell, taste, or thought of  food. About 30% of total acid secretion occurs BEFORE food enters the stomach. These sensory and mental  inputs converge on the hypothalamus, which relays signals to the medulla oblongata. Vagus nerve fibers from  the medulla stimulate the parasympathetic nervous system of the stomach which, in turn, stimulates gastric  secretion (via parietal and G cells).  

∙ Chain of Events 

o Sensory stimuli from food activate dorsal motor nucleus of vagus nerve in the medulla (activating  the parasympathetic nervous system). Insulin induced hypoglycemia also stimulates the vagus nerve.  This results in four distinct physiological events. 

1.) In the body of the stomach, the vagal postganglionic muscarinic nerves  

release acetylcholine(ACh) which stimulates parietal cell H+ secretion. 

2.) In the lamina propria of the body of the stomach the ACh released from the vagal endings  triggers histamine secretion from ECL cells. Histamine also stimulates H+ secretion from  parietal cells. 

3.) In the antrum, peptidergic postganglionic parasympathetic vagal neurons and other  enteric nervous system neurons release GRP which stimulates antral G cellsto produce and  release gastrin. Gastrin stimulates acid secretion by directly stimulating parietal cells as well  as by promoting histamine secretion by ECL cells. 

4.)In both the antrum and corpus, the vagus nerve inhibits D cells, thus reducing their  

release of somatostatin and reducing background inhibition of gastrin release.  

∙ Activation of Gastric Chief Cells 

o Gastric chief cells are primarily activated by ACh. However the decrease in pH caused by activation of  parietal cells further activates gastric chief cells. Alternatively, acid in the duodenum can stimulate S  cells to secrete secretin which acts on an endocrine path to activate gastric chief cells. 

∙ Gastric Phase 

o 50-60% of total gastric acid secretion occurs during this phase. 

o The gastric phase is a period in which swallowed food and semidigested protein (peptides and amino  acids) activate gastric activity. Ingested food stimulates gastric activity in two ways: by stretching the  stomach and by gastric contents stimulating receptors in the stomach. Stretch activates two reflexes:  a short reflex mediated through the myenteric nerve plexus, and a long reflex mediated through the  

vagus nerves and brainstem. 

∙ Distention (Stretching) Path 

1.) Vagovagal Reflex Distention activates an afferent pathway which in turn stimulates efferent  response from the dorsal nucleus of the vagus nerve. Stimulation of acid secretion occurs as it does in  the cephalic phase. 

2.) Local ENS Pathway Activated ENS releases ACh stimulating parietal cells to secrete acid. ∙ Chemical Activation 

o As dietary protein is digested, it breaks down into smaller peptides and amino acids, which directly  stimulate the G cells to secrete even more gastrin – a positive feedback loop that accelerates protein  digestion. As discussed earlier gastrin stimulates by activating parietal cells and stimulating ECL to  produce histamine (histamine stimulates parietal cells to produce acid). Small peptides also buffer  stomach acid so the pH does not fall excessively low.

Study Guide for Exam 4

o Gastric secretion is stimulated chiefly by three chemicals: acetylcholine (ACh), histamine, and gastrin.  ACh is secreted by parasympathetic nerve fibers of both the short and long reflex  

pathways. Histamine is a paracrine secretion from the enteroendocrine cells in the gastric  glands. Gastrin is a hormone produced by enteroendocrine G cells in the pyloric glands. o All three of these stimulate parietal cells to secrete hydrochloric acid and intrinsic factor. The chief  cells secrete pepsinogen in response to gastrin and especially Ach, and ACh also stimulates mucus  secretion. 

∙ Inhibitory Pathway 

o Low intragastric pH stimulates antral D cells to release somatostatin. Somatostatin inhibits gastrin  release from G cells. Reduced gastrin secretion reduces acid secretion. 

∙ Intestinal Phase 

o 5-10% of gastric secretion occurs during this phase. 

o The intestinal phase is a stage in which the duodenum responds to arriving chymeand moderates  gastric activity through hormones and nervous reflexes. The duodenum initially enhances gastric  secretion, but soon inhibits it. 

∙ Duodenal Stimulation of Gastric Secretion 

o Presence of partially digested proteins and amino acids in the duodenum stimulates acid secretion in  the stomach by three methods: 

1.) Peptones stimulate duodenal G Cells to secrete gastrin. 

2.) Peptones stimulate an unknown endocrine cell to release an additional humoral signal,  "enterooxytonin". 

3.) Amino Acids absorbed by the duodenum stimulate acid secretion by unknown mechanisms. ∙ Duodenal Inhibition of Gastric Secretion 

o The acid and semi-digested fats in the duodenum trigger the enterogastric reflex – the duodenum sends inhibitory signals to the stomach by way of the enteric nervous system, and  sends signals to the medulla that  

(1) inhibit the vagal nuclei, thus reducing vagal stimulation of the stomach, and 

(2) stimulate sympathetic neurons, which send inhibitory signals to the stomach. 

o Chyme also stimulates duodenal enteroendocrine cells to release secretin and cholecystokinin. They  primarily stimulate the pancreas and gall bladder, but also suppress gastric secretion and motility. o The effect of this is that gastrin secretion declines and the pyloric sphincter contracts tightly to limit  the admission of more chyme into the duodenum. This gives the duodenum time to work on the  chyme it has already received before being loaded with more. 

o The enteroendocrine cells also secrete glucose dependent insulinotropic peptide. Originally called  gastric-inhibitory peptide, it is no longer thought to have a significant effect on the stomach, but to  be more concerned with stimulating insulin secretion in preparation for processing the nutrients  about to be absorbed by the small intestine. 

Role of CCK and secretin on enterogastric reflex, bile secretion , and pancreatic  secretion, regulation and function of the bile, and regulation of pancreatic  secretion.  

∙ the duodenum must control the acidity of the chyme and the presence of fats- how? o the 2 hormones (CKK and secretin); one goes to the gallbladder to secrete bile and the other goes to  the pancreas

▪ one is supposed to produce movement in the gallbladder- CKK (kineme = movement) ▪ secretin goes to the pancreas to promote secretion

∙ it is connected with the pancreas, liver, and gallbladder

∙ bile helps with the fats, and pancreatic juice (lots of bicarbonate) buffers acidity

Study Guide for Exam 4

∙ bile is produced in the liver from cholesterol (not a bad thing!)

∙ bicarbonate will buffer the pH of the acids and is secreted from the pancreas

∙ pancreas secretes inactive enzymes...if they are active then they would digest the  pancreas

∙ Liver and Gallbladder

o Liver - largest gland/organ in the body

o Composed of four lobes:

▪ anteriolateral - right and left lobes (separated by falciform ligament)

▪ posterior - caudate (superior) and quadrate (inferior)

o Superiormost portion of liver fused with diaphragm

o Lesser omentum anchors liver to lesser curvature of stomach

o Hepatic artery and hepatic portal vein (which enter liver at the porta hepatis) and the common bile  duct travel through lesser omentum to reach their destinations

o Right and left hepatic ducts merge to form the common hepatic duct

o The common heptatic duct merges with the cystic duct to form the bile duct

o Liver composed of hexagonal shaped liver lobules containing plates of hepatocytesradiating outward  from a central vein

o Portal triads- surround lobule and contain a hepatic artery, a hepatic vein, and a bile duct o Between hepatocyte plates are capillaries (liver sinusoids) that receive blood from triads and  transport blood into central vein; sinusoids contain Kupfer cells (macrophages)

o Hepatic cells:

▪ process blood-borne nutrients

▪ store fat-soluble vitamins

▪ detoxify substances

o Secreted bile flows through tiny canals called bile canaliculi that run between adjacent hepatocytes  toward the bile duct branches in portal triads

o Bile (cholesterol and derivatives) emulsify fats

o Mechanisms promoting the secretion of bile:

▪ acidic, fatty chyme enters duodenum and causes release of cholecystokinin (CCK) and  secretin from duodenum wall enteroendocrine cells

▪ CCK and secretin enter bloodstream

▪ bile salts and secretin transported via bloodstream stimulate liver to produce bile

▪ vagal stimulation causes weak contractions of gallbladder

▪ CCK causes gallbladder to contract and hepatopancreatic sphincter to relax: bile enters  duodenum

▪ bile salts reabsorbed into blood

∙ Pancreas

o Extends across the abdomen from its tail (abutting the spleen) to its head (encircled by C- shaped  duodenum)

o Contains endocrine cells (alpha and beta) and exocrine cells which produce pancreatic juice o Pancreatic juice drains from centrally located main pancreatic duct that fuses with the bile duct o Smaller accessory pancreatic duct dumps into directly into duodenum

o Gland contains acinar cells with zymogen granules (contain digestive enzymes)

o Pancreatic juice contains alkaline secretions and inactive and active enzymes

o Regulation of pancreatic juice secretion similar to bile secretion

Study Guide for Exam 4

Gastro-iliac, gastro-colic, and defecation reflex  

∙ the presence of food in the stomach causes stimulation of contraction in the further segments (small  intestine) in order to move the content throughout- otherwise there wouldn't be room for more food ∙ this movement is a reflex- starts in the stomach, stimulates the intestines to contract more and push the food  forward = enterogastric reflex; inhibitory to allow digestion to occur

∙ food causes stomach to increase stimulation in the small intestine = gastroenteric reflex ∙ The defecation reflex is an involuntary response of the lower bowels to various stimuli thereby promoting or  even inhibiting a bowel movement. These reflexes are under the control of the autonomic system and play an  integral role in the defecation process along with the somatic system that is responsible for voluntary control  of defecation. The two main defecation reflexes are known as the intrinsic myenteric defecation  reflex and parasympathetic defecation reflex

∙ Intrinsic Myenteric Defecation Reflex 

o The entry of feces into the rectum causes the distention of the rectal wall. This stretching triggers  signals to the descending and sigmoid colon via the myenteric plexus to increase peristalsis. The  myenteric plexus is part of the enteric nervous system which is the gut’s own internal neural network  as discussed under stomach nerves. 

o The peristaltic waves extend all the way to the rectum an anus. In this manner, fecal matter is moved  closer to the anus. When the wave reaches the anus, it causes the internal anal sphincter, which is  always constricted, to relax. This is achieved by inhibitory signals via the myenteric plexus to reduce  sphincter constriction. 

∙ Parasympathetic Defecation Reflex

o The parasympathetic defecation reflex works in essentially the same way as the intrinsic myenteric  defecation reflex but involves parasympathetic nerve fibers in the pelvic nerves. It triggers peristaltic  waves in the descending and sigmoid colon as well as the rectum. It also causes relaxation of the  external anal sphincter. The difference is that the parasympathetic defecation reflex enhances this  process and makes the intrinsic reflex much more powerful. If sufficiently stimulated, it may even  cause the sigmoid colon to completely empty all of its contents in the rectum rapidly.

o The force triggered by the parasympathetic defecation reflex can be powerful enough to result in  defecation, despite conscious efforts to keep the external anal sphincter constricted.

∙ Other Defecation Reflexes

o Apart from the two main defecation reflexes mentioned above, other reflexes can also influence the  defecation process.

▪ Gastrocolic reflex – distention of the stomach while eating or immediately after a meal  triggers mass movements in the colon.

▪ Gastroileal reflex – distention of the stomach while eating or immediately after eating  triggers the relaxation of the ileocecal sphincter and speeds up peristalsis in the ileum (end  portion of the small intestine). This causes the contents of the ileum to rapidly empty into  the colon.

▪ Enterogastric reflex – distention and/or acidic chyme in the duodenum slows stomach  emptying and reduces peristalsis.

▪ Duodenocolic reflex – distention of the duodenum a short while after eating triggers mass  movements in the colon.

Study Guide for Exam 4

o Irritation within the stomach or duodenum can stimulate or even inhibit the defecation reflexes. In  addition to these gastrointestinal reflexes, there are other reflexes involving the peritoneum, kidney  and bladder that can affect the defecation process. This includes the :

▪ Peritoneointestinal reflex involving the peritoneum and intestines.

▪ Renointestinal reflex involving the kidney and intestines.

▪ Vesicointestinal reflex involving the bladder and intestines.

o When these organs are irritated and the reflexes are triggered, it inhibits intestinal activity. Chemical digestion by salivary amylase, pepsin, pancreatic enzymes: amylase,  lipase, trypsin. Activation of trypsin.

∙ once the enzymes reach the duodenum...

o trypsinogen (inactive) transferred to trypsin (active)

∙ Protein digestion occurs in the stomach and the duodenum through the action of three primary enzymes: o Pepsin, secreted by the stomach.

o Trypsin, secreted by the pancreas.

o Chymotrypsin, secreted by the pancreas.

∙ These enzymes break down food proteins into polypeptides that are then broken down by various  exopeptidases and dipeptidases into amino acids. The digestive enzymes, however, are secreted mainly as  their inactive precursors, the zymogens.

o Thus, trypsin is secreted by the pancreas in the form of trypsinogen, which is activated in the  duodenum by enterokinase to form trypsin. Trypsin then cleaves proteins into smaller polypeptides. ∙ In humans, dietary starches are composed of glucose units arranged in long chains of polysaccharide called  amylose. During digestion, the bonds between glucose molecules are broken by salivary and pancreatic  amylase, and result in progressively smaller chains of glucose. This process produces the simple sugars glucose  and maltose (two glucose molecules) that can be absorbed by the small intestine.

o Sucrase is an enzyme that breaks down disaccharide sucrose, commonly known as table sugar, cane  sugar, or beet sugar. Sucrose digestion yields the sugars fructose and glucose, which are readily  absorbed by the small intestine.

o Lactase is an enzyme that breaks down the disaccharide lactose into its component parts, glucose and  galactose, that are absorbed by the small intestine. Approximately half the adult population produces  only small amounts of lactase and are therefore unable to eat milk-based foods. This condition is  commonly known as lactose intolerance.

o The digestion of certain fats begins in the mouth, where lingual lipase breaks down short chain lipids  into diglycerides. The presence of fat in the small intestine produces hormones that stimulate the  release of pancreatic lipase from the pancreas, and bile from the liver, to enable the breakdown of

Study Guide for Exam 4

fats into fatty acids. The complete digestion of one molecule of fat (a triglyceride) results in three  fatty acid molecules and one glycerol molecule.

∙ DNA and RNA are broken down into mononucleotides by the nucleases deoxyribonuclease and ribonuclease  (DNase and RNase), which are released by the pancreas.

Absorption of specific nutrients: carbohydrates, proteins, and lipids. Mechanisms  to cross apical basolateral membranes. Nutrients diffusing to blood or lymphatic  vessels. (https://quizlet.com/70149654/phy-12-flash-cards/)

∙ digestion of PRO starts in the stomach with the enzyme pepsin, then in the duodenum by trypsin to break  down the peptides into amino acids so that we can absorb them; they have to be in their simplest form

o the amino acid is secondary active transported with Na+

o facilitated diffusion are used with a peptide transporter

o no energy used in facilitated diffusion (at the basement membrane level)

∙ there is similar absorption for CHO and amino acids; when they leave the epithelial cells they go to the blood ∙ Digestion and absorption of Fats

o first we need bile- produced by the liver and stored in the gallbladder (the liver can work without a  bile)

o the bile cuts the globule into smaller globules

▪ the bile exposes more area for the digestive enzymes to work, causing the lipases to become  more active

▪ the bile will transport the fat in the inside to the surface of the epithelial cells and then  continues in the lumen; some is reabsorbed and some is excreted (gives color to the feces) o now that the bile did its work, the pancreatic lipases continue the breakdown of the fats o triglyceride = 3 fatty acids attached to a glycerol molecule

o the lipases cleave one fatty acid = 1 f.a. + 1 diglyceride

o does it again = 2 f.a. + 1 monoglyceride

o chylomicrons- membrane covering all kinds of fats; secreted to the lymph

o fats are not secreted to the blood, they are secreted to the lymph

o the lymph will drain to a vein in the thorax, causing fats to then enter the blood

∙ The small intestine is the part of the gastrointestinal tract between the stomach and the large intestine where  much of the digestion of food takes place. The primary function of the small intestine is the absorption of  nutrients and minerals found in food.

∙ Digested nutrients pass into the blood vessels in the wall of the intestine through a process of diffusion. The  inner wall, or mucosa, of the small intestine is lined with simple columnar epithelial tissue. ∙ Structurally, the mucosa is covered in wrinkles or folds called plicae circulares—these are permanent features  in the wall of the organ. They are distinct from the rugae, which are non-permanent features that allow for  distention and contraction.

∙ From the plicae circulares project microscopic finger-like pieces of tissue called villi (Latin for shaggy hair). The  individual epithelial cells also have finger-like projections known as microvilli. The function of the plicae  circulares, the villi, and the microvilli is to increase the amount of surface area available for the absorption of  nutrients.

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∙ The thin surface layer appear above the capillaries that are connected to a blood vessel. The lacteal is  surrounded by the capillaries.

∙ Each villus has a network of capillaries and fine lymphatic vessels called lacteals close to its surface. The  epithelial cells of the villi transport nutrients from the lumen of the intestine into these capillaries (amino  acids and carbohydrates) and lacteals (lipids).

∙ The absorbed substances are transported via the blood vessels to different organs of the body where they are  used to build complex substances, such as the proteins required by our body. The food that remains  undigested and unabsorbed passes into the large intestine.

∙ Absorption of the majority of nutrients takes place in the jejunum, with the following notable exceptions: o Iron is absorbed in the duodenum.

o Vitamin B12 and bile salts are absorbed in the terminal ileum.

o Water and lipids are absorbed by passive diffusion throughout the small intestine.

o Sodium bicarbonate is absorbed by active transport and glucose and amino acid co-transport. o Fructose is absorbed by facilitated diffusion.

∙ Epithelia form linings throughout the body. In the small intestine, for instance, the simple columnar epithelium  forms a barrier that separates the lumen from the internal environment of the body (note that the internal  environment in which body cells exist is the extracellular fluidor ECF). The epithelium forms a barrier because cells are linked by tight junctions, which prevent many substances from diffusing between adjacent cells. For  a substance to cross the epithelium, it must be transported across the cell's plasma membranes by membrane  transporters.

∙ Not only do tight junctions limit the flow of substances between cells, they also define compartments in the  plasma membrane. The apicalplasma membrane faces the lumen. In the drawing, the apical plasma  membrane is drawn as a wavy line, because intestinal epithelial cells have a high degree of apical plasma  membrane folding to increase the surface area available for membrane transport (these apical plasma  membrane folds are known as microvilli). The basolateral plasma membrane faces the ECF. Epithelial cells  are able to transport substances in one direction across the epithelium because different sets of transporters  are localized in either the apical or basolateral membranes.

∙ Absorption

o Absorption is the means  

whereby nutrients such as  

glucose are taken into the body  

to nourish cells. Glucose is  

transported across the apical  

plasma membrane of the  

intestine by the sodium-glucose  

cotransporter (purple). Because  

transport of Na+and glucose is  

coupled, we need to add the  

free energy inherent in  

Na+transport to the free energy  

inherent in glucose transport to  

get the overall free energy for  

the process. Just after a meal,  

there will be abundant glucose in

the lumen of the intestine,

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favoring absorption. Towards the end of the absorptive phase of a meal, however, the cotransporter  is still able to move glucose into the cell (uphill against its concentration gradient) because of the  strong Na+concentration gradient. The Na+gradient is established by the Na+/K+-ATPase (red), which  is located on the basolateral membrane. The activity of the cotransporter increases the glucose  concentration inside the cells, allowing glucose to be transported into the ECF via the glucose  transporter (blue). Facilitated diffusion of glucose into the ECF is a passive process, since glucose  flows down its concentration gradient.

∙ Secretion

o About 1500 ml of fluid per day is moved from the extracellular fluid into the lumen of the small  intestine in order to provide lubrication that can protect the epithelium and help with intestinal  motility. The mechanism for fluid secretion is that solutes are moved across the epithelium, which  then draw water into the lumen by osmosis. The rate-limiting and regulated step in intestinal  secretion is the movement of Cl ions across the apical plasma membrane.

o The important proteins involved  

in secretion are diagrammed in  

the figure. First, Cl is  

transported into the epithelial  

cell by a cotransporterexpressed  

on the basolateral membrane.  

As with the previous example,  

the Na+gradient, established by  

the Na+/K+-ATPase, provides the  

energy to power transport of  

ions into the cell (this  

cotransporter moves 2 Cl-, one  

K+, and one Na+ion with each  

round of transport). Cl flows  

down its concentration gradient  

into the lumen via the Cl 

channel CFTR(green) located on  

the apical plasma membrane.  

(Not shown is that Na+also flows  

into the lumen, by a passive mechanism).

∙ Regulation of Secretion

o The CFTR protein is a member of the ATP-binding cassette (ABC)protein family. CFTR is an atypical  ABC protein; like other members of the ABC protein family, it binds ATP, but in this case ATP binding  is used to open an ion channel. Importantly, the CFTR protein also has a regulatory domain that is  phosphorylated by protein kinase A (PKA), also known as cAMP-dependent kinase. Intestinal  secretion is turned on when a regulatory molecule binds a G-protein coupled receptor, causing  the alpha subunit of the G-protein to activate the enzyme adenylyl cyclase. Adenylyl cyclase  produces the second messenger cAMP, which activates PKA to phosphorylate CFTR. The channel  opens when both ATP is bound and the regulatory domain is phosphorylated.

Study Guide for Exam 4

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