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BIOL 302- Reading Notes Exam 2

by: Katy Cook

BIOL 302- Reading Notes Exam 2 BIOL 301

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Katy Cook
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Includes notes for all the readings up to Exam 2 material
Anatomy & Physiology
Dr. Rupa De
Study Guide
Anatomy Physiology Rupa Exam Notes Study Guide
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This 44 page Study Guide was uploaded by Katy Cook on Sunday January 31, 2016. The Study Guide belongs to BIOL 301 at Purdue University taught by Dr. Rupa De in Fall 2015. Since its upload, it has received 45 views. For similar materials see Anatomy & Physiology in Biology at Purdue University.


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Date Created: 01/31/16
Chapter 20 readings  Cardiac Muscle tissue and the cardiac conduction system  Cardiac muscle fibers exhibit branching  Normally one or two centrally located nucleus  Intercalated discs contain desmosomes that hold fibers together and gap junctions which allow action potentials to conduct across fibers  Gap junctions allow entire myocardium of atria or ventricles to contract as a coordinated unit  Mitochondria are large and numerous, transverse tubules located at Z discs 2+  SR is somewhat smaller than muscle fibers  less Ca reserve  Autorhythmic fibers: specialized muscle fibers, self-excitable 1. Act as pacemaker- set rhythm of electrical excitation that causes contraction of the heart 2. Form the cardiac conduction system- network of specialized cardiac muscle fibers that provide a path for each cycle of excitation to progress through the heart  Cardiac action potentials propagate through the conduction system in the following sequence: 1. Begins in the sinoatrial (SA) node in right atrial wall. The SA node cells spontaneously depolarize (pacemaker potential). When the pacemaker potential reaches threshold, triggers action potential through both atria via gap junctions  two atria contract at the same time 2. Action potential conducts along atrial muscle fibers, reaches the atrioventricular (AV) node, AP slows considerably, this delay provides time for atria to empty blood into ventricles 3. Action potential enters atrioventricular (AV) bundle (bundle of His), where AP conducts from the atria to the ventricles 4. AP enters both the right and left bundle branches that extend through the interventricular septum towards the apex of the heart 5. Purkinje fibers conduct the AP at the apex up to the ventricular myocardium, ventricles contract, pushing blood up to the semilunar valves  The SA node is the natural pacemaker (100 bpm)  Nerve impulses from the ANS and hormones modify timing and strength of each heartbeat, but they do not establish the fundamental rhythm  Acetylcholine from parasympathetic nervous system slows SA node pacing to 75 bpm  Action potential occurs in a contractile fiber: 1. Depolarization- contractile fibers have resting membrane potential of -9+ mV. When brought to threshold+ voltage- gated fast Na channels open. Inflow of Na down the electrochemical gradient produces rapid depolarization. Within a few milliseconds, Na channels inactivate 2. Plateau- period of maintain2+ depolarization. Due to opening of voltage-gated slow Ca channels in the sarcolemma. Calcium moves into the cytosol, which causes even more Ca 2+ to pour out of the SR into the cytosol through additional channels in the SR membrane. The increased Ca 2+ concentration triggers contraction. Just before plateau phase, some voltage-gated K channels open, K leaves. Membrane potential is close to 0 mV. 3. Repolarization- recovery of the resting membrane potential. + After a delay+ additional voltage-gated K channels open, outflow of K restores the negative membrane potential. At same time, calcium channels are closing  Epinephrine increases contraction force by enhancing Ca 2+flow into the cytosol  Refractory period- time interval during which a second contraction can’t be triggered, lasts longer than the contraction itself  Cardiac muscle relies almost exclusively on aerobic cellular respiration- oxygen diffuses from blood and is released from myoglobin in muscle fibers  At rest: heart’s ATP comes from oxidation of fatty acids and glucose, small contributions from lactic acid, amino acids, and ketone bodies  During exercise: ATP comes from lactic acid produced by contracting skeletal muscles  Some ATP from creatine phosphate  Sign that myocardial infraction has occurred: presence in blood of creatine kinase, the enzyme that catalyzes phosphate group from creatine phosphate to ADP to make ATP (injured or dying cardiac fibers release CK into the blood)  Electrocardiogram (ECG/EKG) is a recording of electrical currents generated by action potentials  Recorded by an electrocardiograph  Possible to determine if the conducting pathway is abnormal, if the heart is enlarged, damage to certain regions, cause of chest pain  P wave- atria depolarization, spreads from SA node through atria  QRS complex- rapid ventricular depolarization, action potential spreads through ventricular contractile fibers  T wave- ventricular repolarization  Larger P wave indicate enlargement of an atrium  Enlarged Q wave may indicate myocardial infarction  Enlarged R wave indicates enlarged ventricles  T wave flatter than normal when heart receives insufficient oxygen +  T wave elevated in hyperkalemia (high blood K )  Intervals- time span between waves  P-Q interval- conduction time from atrial excitation to ventricular excitation (lengthens if action potential forced to detour around scar tissue caused by disorders like coronary artery disease)  S-T segment- elevated above baseline) in acute myocardial infarction, depressed (below baseline) when heart receives insufficient oxygen  Q-T interval- lengthened by myocardial damage, myocardial ischemia (decreased blood flow) or conduction abnormalities  Helpful to evaluate heart’s response to stress of physical exercise (stress testing)  changes can bee seen on an electrocardiogram  Continuous ambulatory electrocardiography: detects abnormal heart rhythms and inadequate blood flow, activity stored in monitor  Systole- phase of contraction  Diastole- phase of relaxation  Heart rate of 75 bpm: 1. Action potential arises in the SA node, propagates throughout atrial muscle to AV node in 0.03 sec. As atrial fibers depolarize, the P wave appears 2. After P wave begins, atria contract (atrial systole), conduction of action potential slows AV node, the resulting 0.1 sec delay gives atria time to contract 3. Action potential propagates rapidly after entering the AV bundle, 0.2 sec after onset of P wave it has propagated through the bundle branches, Purkinje fibers and entire ventricular myocardium. Depolarization progresses down the septum, up from the apex, out from the endocardial surface, producing the QRS complex (at the same time, atrial repolarization is occurring, masked by QRS) 4. Contraction of ventricular fibers (ventricular systole) begins after QRS complex appears, continues during S-T segment. As contraction proceeds toward the base of the heart, blood is squeezed towards semilunar valves 5. Repolarization of ventricular fibers begins at apex and spreads through ventricle  produces T wave about 0.4 sec after onset of P wave 6. Shortly after T wave begins, ventricles relax (ventricular diastole). By 0.6 sec, ventricular repolarization is complete and fibers relaxed  During the next 0.2 sec, all contractile fibers are relaxed  A 0.8 sec, P wave appears again and cycle repeats  The Cardiac cycle  A single cardiac cycle includes all of the events associated with one heartbeat  Atria and ventricles alternately contract and relax, forcing blood from areas of high pressure to low pressure  Atrial systole: 0.1 sec, atria are contracting 1. Depolarization of SA node causes atrial depolarization (P wave) 2. Atrial depolarization causes atrial systole, forces blood through open AV valves into the ventricles 3. Atrial systole contributes 25 mL of blood into in volume already in each ventricle (105 mL). Thus each ventricle contains about 130 mL of blood at end of its relaxation period called end-diastolic volume (EDV) 4. QRS complex in the ECG marks onset of ventricular depolarization  Ventricular systole: 0.3 sec, ventricles are contracting 5. Ventricular depolarization causes ventricular systole. Pressure rises inside ventricles and pushes blood up against the AV valves, forcing them shut. For about 0.05 sec, both the semilunar (SL) and AV valves are closed. This is the period of isovolumetric contraction  cardiac muscle fibers are contracting and exerting force but not yet shortening 6. Continued contraction of ventricles causes pressure to rise, when left ventricular pressure surpasses aortic pressure at about 80 mmHg, and right ventricular pressure rises above pressure in pulmonary trunk at about 20 mmHg, both SL valves open. Ejection of blood from the heart begins. Period when SL valves are open is ventricular ejection, lasts 0.25 sec. Pressure in the left ventricle continues to rise to about 120 mmHg, and pressure in right ventricle reaches 25-30 mmHg 7. Left ventricle ejects 70 mL blood into aorta and right ventricle ejects 70 mL blood into pulmonary trunk. Volume remaining in each ventricle at end of systole is about 60 mL (end-systolic volume/ESV). Stroke volume is the volume ejected per beat from each ventricle (SV = end-diastolic volume – end-systolic volume). At rest, SV= 130- 60 = 70 mL 8. The T wave marks the onset of ventricular repolarization  Relaxation period: lasts 0.4 sec, atria and ventricles both relaxed 9. Ventricular repolarization causes ventricular diastole, pressure within the chambers fall and blood in aorta and pulmonary trunk begins to flow backward toward regions of lower pressure. Backflowing blood catches in valve cusps and closes the SL valve. The aortic valve closes at pressure of 100 mmHg. Rebound of blood off closed cusps of the aortic valve produces the dicrotic wave on aortic pressure curve. After SL valves close, brief interval when ventricular blood volume does not change because all valves closed  isovolumetric relaxation 10. As ventricles continue to relax, pressure falls. When pressure drops below atrial pressure, AV valves open and ventricular filling begins. Major filling occurs just after AV valves open. At the end of the relaxation period, ventricles are ¾ full. P wave appears, signaling start of another cycle  Auscultation- act of listening to sounds within the body  Sound of heartbeat comes from blood turbulence caused by closing of heart valves  During each cycle, there are four heart sounds, but in a normal heart only the first and second (S1 and S2) are loud enough to be heard  S1- lubb sound, is louder and bit longer than S2, caused by closure of AV valve after ventricular systole  S2- dupp sound, shorter and not as loud as S1, caused by closure of closure of the semilunar valves at beginning of ventricular diastole  S3 due to rapid ventricular filling  S4 due to blood turbulence during atrial systole  Heart murmur- heard before, between, or after normal heart sounds - Stenosis: heart murmur heard while valve should be open but is not, mitral stenosis produces murmur between S2 and next S1 - Mitral incompetence: valve should be fully closed but is not, occurs during ventricular systole between S1 and S2  Cardiac output  Cardiac output (CO) is volume of blood ejected from left ventricle (or right ventricle) into the aorta (or pulmonary trunk) each minute  Cardiac output equals the stroke volume (SV), the volume of blood ejected by the ventricle during each contraction, multiplied by the heart rate (HR), the number of heartbeats per minute  CO = SV x HR  Average CO = 5.25 L/min  Factors that increase SV or HR normally increase CO  During mild exercise CO may increase to 10L/min  During intense exercise CO increases to 19.5 L/min  Cardiac reserve is the difference between a person’s maximum CO and CO at rest  If more blood returns to the heart during diastole, more blood is ejected during the next systole  Three factors regulate stroke volume and ensure the left and right ventricles pump equal volumes of blood 1. Preload (degree of stretch on the heart before it contracts) 2. Contractility (forcefulness of contraction) 3. Afterload (the pressure that must be exceeded before ejection of blood from the ventricles can occur)  A greater preload on cardiac fibers prior to contraction increases the force of contraction  the more the heart fills with blood during diastole, the greater the force of contraction during systole)  Frank-starling law of the heart  Preload is proportional to EDV  Two factors determine EDV: 1. Duration of ventricular diastole 2. Venous return (volume of blood returning to the right ventricle)  Contractility: the strength of contraction at any given preload 1. Positive ionotropic agents increase contractility 2. Negative ionotropic agents decrease contractility  Positive ionotropic agents promote Ca 2+ inflow during cardiac action potentials  Stimulation of sympathetic division, hormones such2+s epinephrine and NE, drug digitalis increase Ca level in interstitial fluid  Inhibition of sympathetic division, anoxia, acidosis, some + anesthetics, increased K level in interstitial fluid have negative ionotropic effects  Calcium channel blockers- drugs that have negative ionotropic effect by reducing Ca 2+  The higher the pressure in the ventricles causes blood to push the SL valves open. The pressure that must be overcome before a SL valve can open is termed the afterload  Increase in afterload causes SV to decrease, so more blood remains in ventricles at end of systole  Hypertension and narrowing of arteries by atherosclerosis increase the afterload  Stroke volume may fall if the ventricular myocardium is damaged or if blood volume is reduced by bleeding  Most important regulators of HR are the ANS and hormones released by the adrenal medullae (epinephrine and NE)  Nervous system regulation of the heart originates in the cardiovascular center in the medulla oblongata  receives input from limbic system and cerebral cortex  Proprioceptors that monitor position of limbs and muscles send impulses at increased frequency to the cardiovascular center during exercise  Chemoreceptors monitor chemical changes in blood  Baroreceptors monitor stretching of major arteries and veins  Cardiac accelerator nerves from the thoracic region of the spinal cord extend to the SA node, the AV node, and most portions of the myocardium  trigger release of NE that bind to beta-1 receptors on cardiac muscle fibers 1. In SA and AV node fibers, NE speeds rate of spontaneous depolarization so that these pacemakers fire impulses more rapidly, HR increases 2. In contractile fibers, NE enhances Ca 2+ entry through voltage- 2+ gated slow Ca channels, increasing contractility  Only at very high heart rates does SV decrease due to short filling time  Vagus (X) nerves terminate in the SA node, AV node, and atrial myocardium - Release ACh which decreases HR by slowing rate of spontaneous depolarization  Hormones: - Epinephrine and NE enhance heart’s pumping effectiveness - Increase HR and contractility - Exercise, stress, excitement cause adrenal medullae to release more hormones - Thyroid hormones also enhance contractility and HR - Tachycardia: elevated resting heart rate (sign of hyperthyroidism)  Cations- ionic imbalances can compromise pumping effectiveness + 2+ - Excess Na +locks Ca inflow, decreasing force of contraction - Excess K blocks generation of action potentials - A moderate increase in interstitial Ca 2+levels speed HR and strengthens heartbeat  Age, gender, physical fitness, body temp influence resting heart rate  Bradycardia- slow resting heart rate under 50 bpm  Hypothermia- person’s body is deliberately cooled to low core temperature, slows metabolism that reduces oxygen needs of tissue  Exercise and the heart  Aerobics elevates CO and accelerates metabolic rate  Physiological cardiomegaly: exercise causes hypertrophy of the heart  Pathological cardiomegaly: related to significant heart disease  Help for failing hearts  A cardiac transplant: the replacement of a severely damaged heart with a normal heart from a donor - Patient must remain on immunosuppressant drugs to prevent rejection  Development of atherosclerotic plaques - Excessive amounts of LDL promote atherosclerosis - As a result of tissue damage, blood vessels dilate, increase permeability, phagocytes (macrophages) appear in large numbers  inflammation - LDLs accumulate in inner layer of artery wall, lipids and proteins in LDL undergo oxidation and proteins bind to sugars - Endothelial and smooth muscle cells secrete substances that attract monocytes and convert them to macrophages - Macrophages ingest and become filled with oxidized LDL particles  foam cells - T cells follow monocytes into inner lining of artery where they intensify inflammatory response - Foam cells, macrophages, T cells  fatty streak - Macrophages secrete chemicals that cause smooth muscle cells to migrate to top of plaque, forming cap over it - Heart attack occurs when cap over plaque breaks open  Stress testing- functioning of heart is monitored when placed under physical stress by exercising using a treadmill  ECG recording monitored continuously  Coronary angiography- invasive procedure used to obtain information about the coronary arteries - Catheter inserted into artery toward the heart and into coronary arteries - A radiopaque contrast medium injected into arteries - Angiograms- the radiographs of arteries, appear in motion on a monitor, used to visualize arteries  Coronary artery bypass grafting (CABG)- surgical procedure in which a blood vessel from another part of the body is attached to a coronary artery to bypass an area of blockage  Percutaneous transluminal coronary angioplasty (PTCA)- balloon catheter inserted into an artery, advanced to the point of obstruction, balloonlike device inflated to squash plaque against blood vessel wall - Stent inserted via catheter (metallic, fine wire tube to keep artery open) - Drug-coated coronary stents (drug-eluting) Chapter 21 Readings  Capillaries- the smallest of blood vessels, connect arterial outflow to venous return  Microcirculation: the flow of blood from a metarteriole through capillaries and into a postcapillary venule  Primary function of capillaries is the exchange of substances between the blood and interstitial fluid (also called exchange vessels)  Tissues with high metabolic requirements (muscle, brain, liver, etc.) use more O a2d have extensive capillary networks  Composed of only single layer of endothelial cells and basement membrane  Extensive branching increases the surface area available for rapid exchange of materials  Capillary bed- network of 10-100 capillaries that arise from a single metarteriole  Flow through a capillary network from an arteriole into a venule: 1. Capillaries- blood flows from an arteriole into capillaries, then venules - Precapillary sphincters control blood flow - When sphincters are relaxed (open), blood flows into capillaries - When precapillary sphincters contract, blood flow ceases or decreases - Vasomotion: intermittent contraction and relaxation of smooth muscle of metarterioles and precapillary sphincters - Vasomotion due partly from chemicals released by endothelial cells (nitric oxide) 2. Thoroughfare channel- proximal end of metarteriole is surrounded by scattered smooth muscle fibers whose contraction and relaxation help regulate blood flow - The distal end of the vessel has no smooth muscle  thoroughfare channel - Thoroughfare channel provides a direct route for blood from an arteriole to a venule, thus bypassing capillaries  3 different types of capillaries  Continuous capillaries: plasma membranes of endothelial cells form a continuous tube that is interrupted only by intercellular clefts (gaps between neighboring endothelial cells) - Found in the central nervous system, lungs, muscle tissue, and skin  Fenestrated capillaries- plasma membranes of endothelial cells have many fenestrations (small pores) - Found in kidneys, villi of small intestine, choroid plexus of ventricles in brain, ciliary processes of the eyes, most endocrine glands  Sinusoids- wider and more winding than other capillaries, endothelial cells may have unusually large fenestrations - Incomplete or absent basement membrane, large intercellular clefts - Spleen, anterior pituitary, parathyroid and adrenal glands  Portal vein- blood passes from one capillary network into another (portal system)  Blood distribution  Blood reservoirs- systemic veins and venules, contain a large percentage of blood volume - Blood can be diverted quickly if need arises - Venoconstriction: constriction of veins, reduces volume of blood in reservoirs  Capillary exchange  Capillary exchange- the movement of substances between blood and interstitial fluid  Diffusion- most important method of capillary exchange - O2, CO 2 glucose, amino acids, hormones - Diffuse down concentration gradients into interstitial fluid and into body cells - CO 2nd other wastes released by body cells diffuse into blood - Diffuse through intercellular clefts or fenestrations, lipid- soluble materials may pass across capillary walls directly or through lipid bilayer of endothelial cell plasma membranes - Blood-brain barrier: continuous capillaries blockade movement of materials into and out of brain capillaries  Transcytosis- substances in blood plasma become enclosed within tiny pinocytic vesicles that enter endothelial cells by endocytosis, move across the cell and exit on the other side by exocytosis - Large lipid-insoluble molecules (insulin, certain antibodies)  Bulk flow- passive process in which large numbers of ions, molecules, or particles move together in same direction - Occurs from area of higher pressure to area of lower pressure, continues as long as pressure difference exists - Important for regulation of the relative volumes of blood and interstitial fluid - Filtration: pressure-driven movement of fluid and solutes from blood capillaries into interstitial fluid - Reabsorption: pressure-driven movement from interstitial fluid into blood capillaries  Blood hydrostatic pressure (BHP) and interstitial osmotic pressure promote filtration  Blood colloid osmotic pressure promotes reabsorption  Net filtration pressure (NFP) is the balance of BHP and BCOP- determines whether the volumes of blood and interstitial fluid remain steady or change  Starling’s law of the capillaries: volume of fluid and solutes reabsorbed normally is almost as large as the volume filtered  Blood hydrostatic pressure (BHP) is due to the pressure that water in blood plasma exerts against blood vessel walls - Pushes fluid out of capillaries into interstitial fluid  Interstitial fluid hydrostatic pressure (IFHP) pushes fluid from interstitial spaces back into capillaries (close to zero)  Blood colloid osmotic pressure (BCOP) is a force caused by the colloidal suspension of large proteins in plasma- “pulls” fluid out of capillaries into interstitial fluid  Whether fluids leave or enter capillaries depends on the balance of pressures  NFP = (BHP + IFOP) – (BCOP + IFHP)  NFP= pressure that promote filtration – pressures that promote reabsorption  At arterial end: NFP = (35 + 1) – (26 + 0) = 10 mmHg  net outward pressure, fluid moves out of capillary into interstitial spaces  At venous end of capillary: NFP = (16 + 1) – (26 + 0) = -9 mmHg  net inward pressure, fluid moves into capillary tissue spaces  Every day about 20 L of fluid filter out of capillaries  17 L reabsorbed, 3 L enter lymphatic capillaries  Hemodynamics  Blood flow: volume of blood that flows through any tissue in a given time period (mL/min)  Total blood flow is cardiac output (CO), volume of blood that circulates through systemic or pulmonary blood vessels each minute  CO = HR x SV  CO depends on pressure difference that drives blood through a tissue, and the resistance to blood flow in specific blood vessels  Blood pressure  Greater pressure difference = greater blood flow  Contraction of the ventricles generates blood pressure (BP)- the hydrostatic pressure exerted by blood on the walls of a blood vessel  Blood pressure is determined by CO, blood volume, and vascular resistance  Highest in aorta and large arteries (110/70 is normal)  Systolic BP- highest pressure attained in arteries during systole  Diastolic BP- lowest arterial pressure during diastole  Blood pressure falls as distance from left ventricle increases  Mean arterial pressure (MAP)- average blood pressure in arteries  MAP = Diastolic + 1/3 (S –D)  CO = MAP/resistance  If decrease in blood volume is more than 10% of total, blood pressure drops  Vascular resistance- the opposition to blood flow due to friction between blood and the walls of blood vessels  Depends on size of lumen, blood viscosity, total blood vessel length 1. Size of lumen- smalle4 lumen, greater resistance - Proportional to 1/d - Vasoconstriction narrows the lumen, vasodilation widens it 2. Blood viscosity- depends on ratio of red blood cells to plasma volume, and on concentration of proteins in plasma - Higher viscosity, higher resistance - Dehydration, polycythemia increase blood pressure - Anemia or hemorrhage decreases viscosity  decreases BP 3. Total blood vessel length- directly proportional to resistance, longer = greater resistance - Obese people have hypertension because additional blood vessels in adipose tissue increase blood vessel length  Systemic vascular resistance (SVR)- total peripheral resistance refers to all of the vascular resistances offered by systemic blood vessels  A major function of arterioles is to control SVR by changing their diameters  Main center for regulating SVR is the vasomotor center in the brain stem  Venous return  Venous return- the volume of blood flowing back to the heart through the systemic veins  If pressure increases in the right atrium or ventricle, venous return will decrease - Cause of increased pressure is leaky tricuspid valve  lets blood flow backward as ventricles contract  Skeletal muscle and respiratory pump help pump blood from lower body  Skeletal muscle pump 1. When standing at rest: proximal and distal valves are open, blood flows upward to heart 2. Contraction of leg muscles: compression of vein pushes blood through proximal valve (milking), distal valve closes as some blood is pushed against it 3. Just after muscle relaxation, pressure falls in previously compressed vein, proximal valve closes, distal valve opens because blood pressure in foot is higher than in the leg  vein fills with blood and proximal valve reopens  Respiratory pump - During inhalation, diaphragm moves down which decreases pressure in the thoracic cavity and increase in pressure in abdominal cavity - Abdominal veins compressed, greater volume of blood moves into the decompressed thoracic veins and into the right atrium - When pressures reverse during exhalation, valves in veins prevent backflow from thoracic veins to the abdominal veins  Control of blood pressure and blood flow  Cardiovascular (CV) center in the medulla oblongata helps regulate heart rate and stroke volume  CV center also controls neural, hormonal, and local negative feedback systems to regulate BP and blood flow  Vasomotor center- neurons that regulate HR, contractility of the ventricles, and blood vessel diameter - Proprioceptors: monitor movements of joints and muscles and provide input to the CV center during physical activity - Baroreceptors: monitor changes in pressure and stretch in the walls of blood vessels - Chemoreceptors: monitor concentration of various chemicals in blood  Sympathetic impulses reach the heart via the cardiac accelerator nerves  Parasympathetic stimulation is conveyed along the Vagus (X) nerves, decrease HR  Vasomotor nerves: send impulses to smooth muscle in blood vessel walls, innervate blood vessels in viscera and peripheral areas  Vasomotor tone: moderate state of tonic contraction or vasoconstriction  Neural regulation of blood pressure  Nervous system regulates blood pressure via negative feedback loops  Baroreceptors- located in aorta, internal carotid arteries and other large arteries - Send impulses to CV center to regulate blood pressure - Baroreceptor reflexes: carotid sinus reflex and aortic reflex  Carotid sinus reflex- helps regulate blood pressure in brain  Carotid sinuses- small widening of right and left internal carotid arteries just above where they branch from common carotid arteries  Nerve impulses propagate over sensory axons in the glossopharyngeal (IX) nerves  Aortic reflex- regulates systemic blood pressure via vagus (X) nerves  When blood pressure falls, baroreceptors are stretched less and send nerve impulses at a slower rate to the CV center - CV center decreases parasympathetic stimulation and increases sympathetic stimulation - Increases secretion of epinephrine and NE by adrenal medulla - Heart beats faster, more forcefully, SVR increases, CO rises, BP increases to normal level  When increase in blood pressure, baroreceptors send impulses at a faster rate - CV center increases parasympathetic stimulation, decreases sympathetic stimulation - Decrease in HR, force of contraction, reduction in CO - Vasodilation lowers SVR  Chemoreceptors monitor chemical composition of blood, located in carotid bodies and aortic bodies close to baroreceptors  Chemoreceptors detect changes in O , CO , 2nd H2 + - Hypoxia: low O a2ailable - Acidosis: increase in H concentration - Hypercapnia: excess Co 2  Changes in chemical composition causes CV center to increase sympathetic stimulation to arterioles and veins, producing vasoconstriction and increase in BP - Also provide input to respiratory center to adjust breathing rate  Hormonal regulation of blood pressure  Renin-Angiotensin-Aldosterone (RAA) system - When blood volume falls or blood flow to kidneys decrease - Cells in kidney secrete renin into blood stream - Renin and ACE (angiotensin-converting enzyme) act to produce angiotensin II - Angiotensin II is a potent vasoconstrictor, raises BP by increasing SVR - Angiotensin II stimulates secretion of aldosterone, which increases reabsorption of Na and water by kidneys  increases total blood volume, which increases BP  Epinephrine and NE - Adrenal medulla releases in response to sympathetic stimulation - Hormones increase CO by increasing rate and FOC - Cause vasoconstriction of arterioles and veins in skin and abdominal organs - Vasodilation of arterioles in cardiac and skeletal muscle which increases blood flow to muscle during exercise  Antidiuretic hormone (ADH) - Produced by hypothalamus, released from posterior pituitary in response to dehydration or decreased blood volume - Causes vasoconstriction, which increases BP - Vasopressin is another name for ADH - Promotes movement of water into the bloodstream, which increases blood volume, decreases urine output  Atrial natriuretic peptide (ANH) - Released by cells in atria, ANP lowers blood pressure by causing vasodilation and promoting loss of salt and water in urine to reduce blood volume  Autoregulation of blood flow  When vasodilators dilate arterioles and relax precapillary sphincters, blood flow into capillary networks is increased, which increases O l2vels  Autoregulation: ability of a tissue to automatically adjust its blood flow to match metabolic demands 1. Physical changes - Warming promotes vasodilation, cooling causes vasoconstriction - Myogenic response: smooth muscle in arteriole walls contract more forcefully when stretched, relaxes when stretching lessens 2. Vasodilating and vasoconstricting chemicals - Vasodilating chemicals: K , H , lactic acid, and adenosine, NO - Tissue trauma or inflammation causes release of histamine - Vasoconstricting chemicals: thromboxane A2, superoxide radicals, serotonin, endothelins  Walls of blood vessels in the systemic circulation dilate in response to low O 2  Walls of blood vessels in the pulmonary circulation constrict in response to low levels of O 2  Shock and Homeostasis  Shock is a failure of the cardiovascular system to deliver enough O 2nd nutrients to meet cellular metabolic needs - Cells switch to anaerobic production of ATP, lactic acid accumulates, cells and organs become damaged and may die  Hypovolemic shock- decreased blood volume - Can be caused by acute hemorrhage - Loss of body fluids through sweating, diarrhea, or vomiting - Excessive loss of fluid in urine, inadequate intake of fluid - Venous return to heart declines, filling of the heart lessens, SV decreases, CO decreases  Cardiogenic shock- poor heart function - Most often due to myocardial infarction - Poor perfusion of the heart (ischemia), heart valve problems, excessive preload or afterload, impaired contractility of muscle fibers, arrhythmias  Vascular shock- inappropriate vasodilation - Anaphylactic shock: severe allergic reaction, release of histamines that cause vasodilation - Neurogenic shock: trauma to head that causes malfunction of CV center - Septic shock: stems from bacterial toxins that produce vasodilation  Obstructive shock- obstruction of blood flow - Pulmonary embolism: blood clot lodged in blood vessel of the lungs  Homeostatic responses to shock  Compensatory mechanisms can maintain adequate blood flow and blood pressure in as much as 10% of total volume blood loss 1. Activation of the RAA system- decreased blood flow to kidneys causes kidneys to secrete renin, angiotensin II causes vasoconstriction, stimulates adrenal cortex to secrete aldosterone, increase in SVR and blood volume 2. Secretion of ADH- posterior pituitary releases more ADH to conserve remaining blood volume, causes vasoconstriction to increase SVR 3. Activation of sympathetic division of ANS- baroreceptors initiate sympathetic response, vasoconstriction of arterioles and veins, increases SVR, constriction of veins increases venous return, increase in HR, contractility, epinephrine and NE intensify vasoconstriction and increase HR and contractility 4. Release of local vasodilators: cells liberate K , H , lactic acid, adenosine, and NO to increase blood flow and restore O to 2 parts of the body  Signs and symptoms of shock - Systolic blood pressure lower than 90 mmHg - Rapid resting HR - Weak pulse due to reduced CO and fast HR - Skin cool, pale, and clammy due to constriction of blood vessels - Mental state altered due to reduced oxygen supply to brain - Urine reduced - Thirsty - pH of blood is low due to buildup of lactic acid - Nausea due to impaired blood flow to digestive organs Chapter 19 readings  Functions and properties of blood  Blood: a liquid connective issue that consists of cells surrounded by a liquid extracellular matrix called blood plasma  Interstitial fluid: fluid that bathes body cells and is constantly renewed by the blood  Blood transports oxygen from the lungs and nutrients from the GI tract which diffuse into the interstitial fluid and into body cells  Carbon dioxide and wastes move from body cells to interstitial fluid to blood  Blood transports waste to lungs, kidneys, skin, etc. for elimination  Functions of the blood 1. Transportation: transports oxygen, carbon dioxide, nutrients, hormones, as well as heat and waste to organs for elimination 2. Regulation: circulating blood helps maintain homeostasis of all body fluids - Helps regulate pH through use of buffers, adjust body temp through heat-absorbing and coolant properties of water in blood plasma - Blood osmotic pressure influences water content of cells through interactions of dissolved ions and proteins 3. Protection: blood can clot against its excessive loss after an injury, white blood cells protect against disease (antibodies, interferons, complement)  Physical characteristics of blood  Blood is more viscous than water and feels slightly sticky  Slightly alkaline, 38 degrees Celsius  Bright red with saturated with oxygen, dark red when unsaturated  20% of extracellular fluid, 8% total body mass  5-6 L in males, 4-5 L in females  Aldosterone, ADH, ANP regulate how much water is excreted in urine to monitor blood volume and osmotic pressure  Blood has two components: blood plasma (watery liquid extracellular matrix that contains dissolved substances) and formed elements (cells and cell fragments)  45% formed elements, 55% blood plasma  Buffy coat: layer of white blood cells and platelets between the packed RBCs and plasma in centrifuged blood  Blood plasma - 91.5% water, 8.5% solutes (mostly proteins) - Plasma proteins: proteins confined to blood - Hepatocytes synthesize most of plasma proteins (albumins, globulins, fibrinogen) - Antibodies- gamma globulins or immunoglobulins - An antibody binds specifically to the antigen that stimulated its production - Other solutes include electrolytes, nutrients, regulatory substances, hormones, gases, waste products  Formed Elements- red blood cells, white blood cells, platelets - Red blood cells: erythrocytes, transport oxygen from lungs to body cells and deliver carbon dioxide from body cells to lungs - White blood cells: leukocytes, protect body from invading pathogens  neutrophils, basophils, eosinophils, monocytes, lymphocytes (B & T) - Platelets: fragments of cells with no nucleus, release chemicals that promote blood clotting  Hematocrit: percent of total blood volume occupied by RBCs (normal range = 38-46% in females, 40-54% in males)  Testosterone stimulates synthesis of erythropoietin (EPO) that stimulates production of RBCs  Anemia- lower than normal number of RBCs  Polycythemia- percent of RBCs is abnormally high  increases viscosity, high blood pressure, risk of stroke  Blood doping- use of EPO by athletes  Formation of blood cells  Hemopoiesis: process by which formed elements of blood develop  Red bone marrow becomes primary site of hemopoiesis  Red bone marrow: highly vascularized connective tissue between trabeculae of spongy bone tissue  0.05%-0.1% of red bone marrow cells are pluripotent stem cells (hemocytoblasts) derived from mesenchyme - Cells have capacity to develop into many different types of cells - Stem cells in red bone marrow reproduce themselves, proliferate, and differentiate into cells that give rise to blood cells, macrophages, reticular cells, mast cells, and adipocytes  Reticular cells produce reticular fibers which form the stroma that supports red bone marrow cells  Blood from nutrient and metaphyseal arteries enters a bone and passes into the sinuses (enlarged & leaky capillaries) that surround bone marrow cells & fibers  After blood cells form, they enter sinuses and other blood vessels and leave bone through nutrient and periosteal veins  Formed elements (except lymphocytes) do not divide once they leave bone marrow  Myeloid stem cells- give rise to RBCs, platelets, monocytes, neutrophils, eosinophils, basophils, and mast cells  Lymphoid stem cells give rise to lymphocytes  Progenitor cells- no longer capable of reproducing themselves, committed to giving rise to more specific elements of blood  Colony-forming unites (CFUs)- designates the mature elements in blood that they will produce  Precursor cells (also known as blasts)- over several cell divisions develop into formed elements of blood  Hemopoietic growth factors- regulate differentiation and proliferation of progenitor cells  Erythropoietin (EPO) increases the number of RBC precursors  Thrombopoietin (TPO) is a hormone produced by the liver that stimulates formation of platelets from megakaryocytes  Cytokines: small glycoproteins typically produced by red bone marrow cells, leukocytes, macrophage, fibroblasts, and endothelial cells - Stimulate proliferation of progenitor cells in red bone marrow and regulate activities of cells involved in nonspecific defenses and immune responses - Colony-stimulating factors (CSFs) and interleukins stimulate WBC formation  Red Blood Cells  Erythrocytes, contain oxygen-carrying protein hemoglobin which gives blood its red color  4.8-5.4 million RBCs/ microliter of blood  Biconcave discs, plasma membrane strong and flexible which allows them to deform without rupturing as they squeeze through narrow capillaries  Lack nucleus and other organelles, cytosol contains hemoglobin  Highly specialized for their oxygen transport function  RBCs lack mitochondria and generate ATP anaerobically so they don’t use up any oxygen they transport  Each RBC contains 280 million hemoglobin molecules  Globin is a protein composed of four polypeptide chains (2 alpha, 2 beta) and ringlike nonprotein pigment called a heme at each chain 2+  At the center of each heme ring is an iron ion (Fe ) that can combine reversibly with one oxygen molecule  Each hemoglobin binds four oxygen molecules  23% of carbon dioxide is transported by hemoglobin which combines with amino acids in the globin  Hemoglobin also regulates blood flow and blood pressure  Nitric oxide produced by endothelial cells that line blood vessels binds to hemoglobin  if released, NO causes vasodilation which improves blood flow and enhances oxygen delivery  Red blood cells contain enzyme carbonic anhydrase (CA) which catalyzes conversion of carbon d+oxide and w-ter to carbonic acid which dissociates into H and HCO 3 - Allows carbon dioxide to be transported in blood plasma from tissue cells to lungs in form of HCO 3- - Important buffer in extracellular fluid  RBC lifecycle  Live only about 120 days  Cannot synthesize new components to replace damaged ones  Ruptured blood cells destroyed by phagocytic macrophages in spleen and liver  Recycling occurs as follows: 1. Macrophages in spleen, liver or red bone marrow phagocytize ruptured and worn-out RBCs 2. Globin and heme portions of hemoglobin split apart 3. Globin broken into amino acids to synthesize other proteins 4. Iron removed from heme associates with the plasma protein transferrin that transports iron in the bloodstream 5. In muscle fibers, liver cells, and macrophages of the spleen and liver, Fe3+detaches from transferrin and attaches to an iron-storing protein called ferritin 6. On release from storage site or absorption from the GI tract, Fe3+ reattaches to transferrin 7. The Fe -transferrin complex carried to red bone marrow where RBC precursor cells take it up through endocytosis for hemoglobin synthesis 8. Erythropoiesis in red bone marrow results in production of RBCs 9. When iron removed from heme, the non-iron portion is converted to biliverdin (green pigment) and bilirubin (yellow- orange pigment) 10. Bilirubin enters blood and transported to liver 11. Bilirubin released by liver cells into bile, which passes into large intestine 12. Bacteria converted bilirubin into urobilinogen 13. Urobilinogen absorbed back into blood, converted to yellow pigment called urobilin and excreted in urine 14. Most urobilinogen eliminated in feces in the form of a brown pigment called stercobilin  Erythropoiesis- production of RBCs starts in red bone marrow with precursor cell called a proerythroblast  Proerythroblast divides several times, producing cells that begin to synthesize hemoglobin  Cell near the end of development ejects its nucleus and becomes a reticulocyte (causes indentation)  enters bloodstream by squeezing between the endothelial cells of blood capillaries  develop into mature red blood cells within 1-2 days  Hypoxia- cellular oxygen deficiency may occur if too little oxygen enters the blood - Stimulates kidneys to step up release of erythropoietin (speeds up development of proerythroblasts into reticulocytes in red bone marrow) - As number of RBCs increases, more oxygen delivered to body tissues  Stem Cell transplants from bone marrow and cord blood  Bone marrow transplant: replacement of cancerous or abnormal red bone marrow with health red bone marrow in order to establish normal blood cell counts  Bone marrow may be supplied by a donor or the patient when the underlying disease is inactive (in remission)  Bone marrow transplants used to treat aplastic anemia, leukemia, SCID, Hodgkin’s disease, etc.  Patient extremely vulnerable to infection because WBCs destroyed by chemotherapy and radiation  Graft-versus-host disease: transplanted marrow produces T cells that attack recipient’s tissues  Patients must take immunosuppressive drugs  Cord-blood transplant - Stem cells obtained from umbilical cord after birth, removed, and frozen 1. Easily collected following permission of newborn’s parents 2. More abundant than red bone marrow stem cells 3. Less likely to cause graft-versus-host disease 4. Less likely to transmit infections 5. Can be stored indefinitely in cord-blood banks  Hemostasis  Hemostasis: sequence of responses that stops bleeding  When blood vessels damaged or ruptured, response must be quick, localized and carefully controlled  3 mechanisms reduce blood loss: vascular spasm, platelet plug formation, blood clotting  Hemostasis prevents hemorrhage  Vascular spasm- circularly arranged smooth muscle in walls of arteries or arterioles contracts immediately - Reduces blood loss for several minutes-hours - Caused by damage to smooth muscle, substances released from activated platelets, and reflexes initiated by pain receptors  Platelet Plug formation - Platelet-derived growth factor (PDGF) is a hormone that can cause proliferation of vascular endothelial cells, vascular smooth muscle fibers, and fibroblasts to help repair damaged blood vessels 1. Platelets contact and stick to parts of damaged vessel  platelet adhesion 2. Platelets become activated, extend many projections that enable them to contact and interact w/ one another, begin to liberate contents of their vesicles  platelet release reaction (ADP and thromboxane A2 activate nearby platelets, serotonin and thromboxane A2 function as vasoconstrictors 3. Release of ADP makes other platelets in the area sticky  platelet aggregation - Eventually the accumulation and attachment of large numbers of platelets form a mass called a platelet plug - Becomes tight when reinforced by fibrin threads, can stop blood loss completely if hole in blood vessel is not too large  Blood clotting- blood thickens and forms gel when drawn from body - Gel separates from liquid (serum) - The gel is called a blood clot, consists of network of insoluble protein fibers called fibrin in which formed elements of blood are trapped  Clotting (coagulation): process of gel formation  Thrombosis: if blood clots too easily, clotting in undamaged blood vessel  Clotting factors: Ca , inactive enzymes synthesized by hepatocytes, and various molecules associated w/ platelets or released by damaged tissues  Clotting is a complex cascade of enzymatic reactions until large quantity of fibrin is formed  Clotting can be divided into three stages (2 and 3 = common pathway): 1. Extrinsic and intrinsic pathway lead to formation of prothrombinase 2. Prothrombinase converts prothrombin into the enzyme thrombin 3. Thrombin converts soluble fibrinogen into insoluble fibrin (fibrin forms the threads of the clot)  Extrinsic pathway- occurs rapidly, tissue factor (TF) also known as thromboplastin leaks into blood from cells outside (extrinsic to) blood vessels - In presence of Ca , TF begins a sequence of reactions that ultimately activates clotting factor X which combines with factor V to form prothrombinase  Intrinsic pathway- occurs more slowly - Activators are in direct contact with blood or contained within blood - Damaged endothelial cells cause damage to platelets which release phospholipids - Contact with collagen fibers activates clotting factor XII that eventually activates clotting factor X  combines with factor V to form prothrombinase  The common pathway - Begins with formation of prothrombinase - Prothrombinase and Ca 2+ convert fibrinogen to loose fibrin threads - Thrombin activates factor XIII which strengthens and stabilizes the fibrin threads into a sturdy clot - Thrombin has two positive feedback effects 1. Involves factor V, accelerates formation of prothrombinase, which accelerates production of more thrombin, etc. 2. Thrombin activates platelets, which reinforces their aggregation and the release of platelet phospholipids  Clot retraction- the consolidation or tightening of the fibrin clot - Fibrin threads gradually contract as platelets pull on them, pulls edges of damaged vessel close together - Retraction depends on adequate number of platelets in the clot, which release factor XIII and other factors, strengthening and stabilizing the clot - With time, fibroblasts form connective tissue, and new endothelial cells repair vessel lining  Vitamin K required for synthesis of four clotting factors - Fat soluble vitamin, can be absorbed through lining of intestine and into blood if absorption of lipids is normal  Fibrinolytic system- dissolves small, inappropriate clots; also dissolves clots at site of damage once damage is repaired  Fibrinolysis- dissolution of a clot  Plasminogen- inactive plasma enzyme, incorporated into clot when formed - Body tissues and blood contain substances that can activate plasminogen to plasmin, an active plasma enzyme - Once plasmin is formed it can dissolve clot by digesting fibrin threads and inactivating substances like fibrinogen, prothrombin, and factors V and XII  Clot formation remains localized: fibrin absorbs thrombin into clot, dispersal of clotting factors does not remain at high enough concentration  Prostacyclin- produced by endothelial and WBCs, opposes actions of thromboxane A2, inhibitor of platelet adhesion and release  Anticoagulants: substances that delay, suppress, or prevent blood clotting - Antithrombin- blocks factors XII, X, and II (prothrombin) - Heparin- produced by mast cells and basophils, combines with antithrombin and increases its effectiveness - Activated protein C (APC)- inactivates two major clotting factors and enhances activity of plasminogen activators  Intravascular clots: initiated by roughened endothelial surfaces, induce adhesion of platelets, also form when blood flows too slowly  Thrombosis: clotting in an unbroken blood vessel (usually a vein) - Clot itself is called a thrombus  Embolus: a blood clot, bubble of air, fat from broken bones, or piece of debris transported by the bloodstream  Pulmonary embolism: an embolus that lodges in lungs  Disorders  Sickle cell disease - RBCs contain abnormal kind of hemoglobin - Sickled cells rupture easily  leads to anemia - Do not move easily through blood vessels, tend to stick together and block vessels - Inherited  Hemophilia - Inherited deficiency of clotting in which bleeding may occur spontaneously or after only minor trauma  Leukemia - Group of red bone marrow cancers in which abnormal WBCs multiply uncontrollably - Interferes with production of RBCs, white blood cells, and platelets - Symptoms of anemia  Jaundice: abnormal yellowish discoloration of sclerae of eyes, skin, and mucous membranes due to excess bilirubin in blood  Thalassemia  Hemoglobin and hyperglycemia Chapter 26  Functions of the Kidneys  Regulation of blood ionic composition + + 2+ - 2- - Regulate blood levels of (Na ), (K ), (Ca ), (Cl ), and (HPO ) 4  Regulation of blood pH - Excrete variable amount of H into the urine and conserve bicarbonate ions (HCO ), which are important to buffer H in + 3 the blood  Regulation of blood volume - Conserve or eliminate water in the urine  Regulation of blood pressure - Secrete the enzyme renin, which activates the RAA pathway - Increased renin causes an increase in BP  Maintenance of blood osmolarity - Regulate loss of water and loss of solutes in the urine - Relatively constant blood osmolarity of 300 mOsm/L  Production of hormones - Produce calcitriol (active form of vitamin D, regulates calcium homeostasis) - Erythropoietin stimulates production of red blood cells  Regulation of blood glucose level - Use the amino acid glutamine in gluconeogenesis, can then release glucose into the blood  Excretion of wastes and foreign substances - By forming urine, kidneys help excrete wastes (substances that have no useful function in the body) - Some wastes result from metabolic reactions (ammonia and urea from deamination of amino acids; bilirubin from catabolism of hemoglobin; creatine from breakdown of creatine phosphate; uric acid from catabolism of nucleic acids; drugs and toxins)  Anatomy and Histology  Nephrons are the functional units of the kidneys  Each nephron consists of a renal corpuscle (where blood plasma is filtered), and a renal tubule (into which the filtered fluid passes)  Two components of a renal corpuscle are the glomerulus (capillary network) and the glomerular capsule (a double-walled epithelial cup that surrounds the glomerular capillaries)  Renal tubule consists of 1. Proximal convoluted tubule 2. Nephron loop (loop of Henle) 3. Distal convoluted tubule  Distal convoluted tubules of several nephrons empty into a single collecting duct  Collecting ducts unit and converge into several hundred large papillary ducts which drain into the minor calyces  Juxtamedullary nephrons- have long nephron loops that extend into deepest region of the medulla  Flow of fluid through a cortical nephron - Glomerular (Bowman’s) capsule  PCT  descending limb of the nephron loop  ascending limb of the nephron loop  DCT  A single layer of epithelial cells forms the entire wall of the glomerular capsule, renal tubule, and ducts  Glomerular capsule - Visceral layer consists of modified simple squamous epithelial cells called podocytes (wrap around glomerular capillaries - Parietal layer consists of simple squamous epithelium and forms the outer wall of the capsule  Capsular space- space between two layers of glomerular capsule  Principal cells in the last part of the DCT: have receptors for ADH and aldosterone  Intercalated cells play role in homeostasis of blood pH  Overview of renal physiology  To produce urine, nephrons and collecting ducts perform three basic processes 1. Glomerular filtration - Water and most solutes in blood plasma move across wall of glomerular capillaries, where they are filtered and move into the glomerular capsule and then into the renal tubule 2. Tubular reabsorption - Tubule cells reabsorb about 99% of the filtered water and useful solutes as the filtered fluid flows through the renal tubules and through the collecting ducts. The water and solutes return to the blood as it flows through the pertubular capillaries and vasa recta 3. Tubular secretion - As filtered fluid flows through renal tubules and collecting ducts, the renal tubule and duct cells secrete other materials, such as wastes, drugs, and excess ions into the fluid (secretion removes a substance from the blood)  Urine contains secreted substances  Blood contains reabsorbed substances  Rate of urinary excretion of any solute is equal to its rate of glomerular filtration, plus its rate of secretion, minus rate of reabsorption  Glomerular filtration  Glomerular filtrate: the fluid that enters the capsular space  Filtration fraction: the fraction of blood plasma in the afferent arterioles of the kidneys that becomes glomerular filtrate  More than 99% of glomerular filtrate returns to blood via tubular reabsorption, so only 1-2 L is excreted as urine  Filtration membrane: leaky barrier composed of glomerular capillaries and the podocytes which encircle the capillaries - Permits filtration of water and small solutes, prevents filtration of most plasma proteins, blood cells, and platelets  Substances filtered from the blood cross three filtration barriers 1. Glomerular endothelial cells - Have large fenestrations, quite leaky - Prevents filtration of blood cells and platelets - Mesangial cells (among capillaries and in cleft between arterioles), contractile cells help regulate filtration 2. Basal lamina - Acellular material between endothelium and the podocytes, consists of collagen fibers and proteoglycans in a matrix - Negative charges in the matrix prevent filtration of larger negatively charged plasma proteins 3. Filtration slit formed by a podocyte - Pedicels are footlike processes that extend from each podocyte, wrap around glomerular capillaries - Space between them= filtration slits - Slit membrane extends across each filtration slit, permits passage of small molecules (water, glucose, vitamins, amino acids, small plasma proteins, ammonia, urea, ions)  Volume of fluid filtered by renal corpuscle is much larger than in other blood capillaries - Glomerular capillaries present a large surface area, mesangial cells regulate how much surface area is available (maximal when relaxed, high filtration) - Filtration membrane is thin and porous - Glomerular capillaries are 50 times leakier than blood capillaries - Glomerular capillary blood pressure is high  efferent arterioles is smaller in diameter than the afferent arteriole, resistance to the outflow of blood from the glomerulus is high  Net filtration pressure (NFP) = GBHP – CHP – BCOP  Glomerular Blood hydrostatic pressure (GBHP)- the blood pressure in glomerular capillaries (55 mmHg), promotes filtration by forcing water and solutes in blood plasma through the filtration membrane  Capsular hydrostatic pressure (CHP)- hydrostatic pressure exerted against the filtration membrane by fluid already in the capsular space and renal tubule, opposes filtration and represents a “back pressure” of about 15 mmHg  Blood colloid osmotic pressure (BCOP)- due to presence of proteins such as albumin, globulins, and fibrinogen in blood plasma, opposes filtration (30 mmHg)  Glomerular filtration rate: the amount of filtrate formed in all renal corpuscles of both kidneys each minute (125 mL/min in males, 105 mL/min in females)  Homeostasis of body fluids requires kidneys maintain a relatively constant GFR (substances are not reabsorbed and are lost in the urine if too high, if too low all the filtrate may be reabsorbed and certain waste products not adequately excreted)  Any change in net filtration pressure will affect GFR  Mechanisms regulate GFR operate by adjusting blood flow into and out of the glomerulus, and by altering the glomerular capillary surface area  GFR increases when blood flow into the glomerular capillaries increase  Control of the diameter of afferent and efferent arterioles regulates blood flow  Constriction of afferent arteriole decreases blood flow, dilation increases it  Three mechanisms to control GFR: renal autoregulation, neural regulation, hormonal regulation  Renal autoregulation  Maintain nearly constant GFR over a wide range of systemic blood pressures  Myogenic mechanism- occurs when stretching triggers contraction of smooth muscle cells in the walls of afferent arterioles  When arterial blood pressure drops, smooth muscle cells are stretched less and relax, afferent arterioles dilate, renal blood flow increases, GFR increases  Tubuloglomerular feedback- macula densa provides feedback to the glomerulus, operates more slowly than myogenic mechanism  When GFR is above normal, filtered fluid flow more rapidly along renal tubules, PCT and nephron loop have less time to reabsorb Na , Cl , and water +


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