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Human Physiology - TEST III.doc

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Department
Human Kinetics
Course
HK 2810
Professor
Coral Murrant
Semester
Fall

Description
Human Physiology Test III FALL 2003 1. Diagram the action potential of a ventricular myocyte and describe the ion movement and channels involved in establishing this action potential. Describe the changes in permeability of potassium throughout the duration of this action potential. What is the importance of these changes in permeability to potassium? Answer: 1) Voltage gated Na+ channel opens and fast influx of Na+ occurs, and quickly inactivated (depolarization) 2) K+ channel opens and K+ diffuses out down the concentration and electrical gradient. (repolarization) 3) Voltage gated Ca2+ channel opens, Ca2+ flux in, therefore depolarization occurs (small) 4) When Ca2+ in = K+ out  plateau 5) Ca2+ in < K+ out as Ca2+ channel starts to inactivate repolarization occurs 6) Na+ channel completely closed (relative refractory period starts) – no Na+ flux 7) Ca2+ channel starts to close and Ca2+ ATPase become active pumping trigger Ca2+ out to extracellular space; 3Na+/1Ca2+ ATPase(pump Ca2+ out, Na+ in) activates, and H+/Ca2+ exchanger works Potassium permeability drops throughout the duration of the AP. The permeability of K+ must drop so we remain depolarized long enough to open enough Ca2+ channel to get ample trigger Ca2+ channel to contract the cardiac cell. If we didn’t decrease K+ permeability, we would repolarize immediately, and decrease Ca2+ flux into the cell  therefore less contraction occurs Diagram) 2. Diagram and describe the events of the cardiac cycle of the left ventricle through diastole and systole showing the relationship between ventricular pressure and ventricular volume. Indicate the changes that would occur in this relationship in the presence of epinephrine Answer: 1) Diastole – ventricular relaxation, blood filling into ventricle occurs (80% of preload) 2) Atrial contraction during the diastole of Ventricle to provide 20% of blood (increased volume, increased pressure) 3) Systole – ventricular contracton (isometric contraction – no change in volume, but increased pressure) 1. mitral valve(Pv>Patrium) and aortic valve(Paorta> Pv) both closed  pressure build up 4) Pv > Paorta  Aortic valve opens and blood gets ejected (120mmHg – systolic pressure) 1. decreased volume 5) Ventricular relaxation  Pv decreases 6) Pv < Paorta  aortic valve closes  Isometric relaxation (no change in volume, but decreased pressure) 7) Patrium > Pv  Mitral valve opens and rapid filling occurs 1. increased volume Epinephrine is released from adrenal gland(endocrine) via SNS activity . Epinephrine binds beta adrenergic Rc and cause G protein conformation change which activated Adenyl Cyclase activity (increased cAMP) Increased cAMP then increase protein kinase activity to phosphorylate voltage gated L type Ca2+ channel on membrane. Increased number of channel opened per AP the increase trigger Ca2+ to increase contractility. Also Ca2+ pumps on SR get phosphorylated, and this results in decreased relaxation time for cardiac muscle and ultimately decreased relaxation time. Therefore Epinephrine increases the force of contraction as well as the speed of contraction. Diagram) 3. There are multiple regulators of vascular smooth muscle function. Discuss the regulation of vascular smooth muscle of arterioles in the heart. Provides an example for each regulator or type of regulation. Describe how an increase in SNS activity would alter the regulation of vascular smooth muscle function in the heart Answer: Neuronal control plays a major role by direct SNS innervation which releases NE to VSM to vasoconstrict VSM releases NO to vasodilate (NO  increased cGMP  vasodilation) in autocrine manner Paracrine From endothelial cells: NO, Endothelin, EDRF, EDCF, EDHF are released to cause vasodilation, and PGI2 to vasoconstrict. Cardiac cell (parachymal cell) releases metabolites such as CO2, H+, K+, phosphate, and adenosine to vasodilate VSM. Adventitial cell secretes NO to vasodilate Endocrine SNS innervation on adrenal gland causes epinephrine release; depending on the membrane receptor population, effects differ  alpha Rm: cause constriction, beta: cause dilation (for example Heart is mainly beta Rm so that it will vasodilate). A II and ADH-VP vasoconstrictors while ANP is vasodilaters which is released in response to stretch in right atria(increased volume) Also Flow shear from RBC cause bending occurs on Rm which will cause 2 messenger release. BK (bradykinin) causes vasodilation Physiological factor (Pt = transmural pressure) also plays a role in regulation of VSM. During contraction of VSM, environmental pressure increases therefore decreasing flow to heart. During the period of decreased flow, vasoactive materials are not released cell and build a gradient. Overshoot of flow occurs when vasoactive material fluxes out. Increased SNS activity would increase the direct nervous input and increase heart rate and contractility therefore increases metabolites from cardiac cells. Also increased SNS to adrenal gland would increase hormonal production (increased Epi level) and change VSM function. 1 4. Standing on your head will result in a sudden drop in glomerular filtration rate (GFR). Describe the processes by which the kidney would immediately restore GFR back to normal. Focus your answer on mechanisms local to the kidney Answer: Decreased GFR is catastrophic, because a little change can cause huge amount of fluid build up in body. Decreased GFR will lead to decreased flow in tubule therefore increased equilibration time. Because equilibration time is increased, more water will move out to ISS to dilute, and Na+ movement down the concentration gradient, Na+, K+, Cl- symporter activity in thick ascending limb of L of H and NaCl- symporter activity in early distal tubule will increase. This results in less NaCl left when it reaches distal tubule (macular densa). Macular densa has chemoRc which shrivel or swell depending on the concentration of NaCl. Product released from macular densa cells onto smooth muscle of afferent arterioles to decrease resistance in the afferent arterioles. This increases glomerulus volume and glomerulus pressure. As glomerulus pressure increases, GFR increases back to normal level. This is called tubuloglomerular feedback Product released from macular densa cells acts to increase renin and local conversion of angiotensiongen (synthesized from liver, inactive, activated by renin) to AI occurs. AI then becomes A II by angiotensin converting enzyme from epithelial cell of afferent arteriole. Increased angiotensin II vasoconstricts efferent more than afferent to increase glomerular pressure. And GFR increases back to normal range 5. You are on the way to the Keg after your physiology test and you fall, hit your head and you are losing blood. Explain how this loss of 500ml of blood volume would immediately affect fluid flux across one of your skeletal muscle capillary beds. When rushed to the hospital you receive a rapid infusion of 500ml of saline(mostly water and no plasma proteins) to increase your blood volume. Explain how this saline infusion would immediately affect fluid flux across one of your skeletal muscle capillary beds Answer: 500ml blood loss It results in decreased MAP from decreased volume in Aorta. Due to decreased MAP, volume into Cap bed decreases, and so does Pc. Since ∆P = Pc – Pt, ∆ P also decreases, while ∆  doesn’t change. ∆P is a hydrostatic drive for flux out of Cap to ISS, while ∆ is an osmotic drive for flux out of ISS to cap. You will have less filtration (from Cap to ISS) and more reabsorption (from ISS to Cap). Increase fluid flux from tissue to the capillary, therefore blood volume increases. Saline infusion Saline has no blood protein but has water. It increases volume in aorta and increase MAP. Volume into Cap bed increases and so does Pc. Since ∆P = Pc-Pt, ∆P also increases.  capillary decreases because saline devoid of plasma protein. Since ∆  =  capillary - tissue, ∆ decreases as well. Therefore, you will have more filtration (from cap to ISS) and less reabsorption (from ISS to cap). Increased fluid flux from capillary to tissue, therefore blood volume decreases 6. It is a very bad day and you are in left heart failure (decrease in contractility of the left heart). Describe how this would affect pressure in the aorta. Explain how this would affect ADH-VP release and describe how these changes in ADH-VP would affect water loss at the kidney Answer: Left heart failure results in decreased aortic pressure because its contractility has decreased (less CO  decreased blood volume in aorta). Decreased pressure in aorta is sensed by high pressure baro Rc (carotid artery and aortic arch; stretch receptor). As MAP decreases, sensor decreases AP firing. It decreases inhibition on ADH-VP release from ADH releasing cells in hypothalamus, and ADH-VP release is increased. ADH adds water channels on basolateral and apical side of distal tubule and collecting duct to increase water permeability (to move it back to blood vessels). Also ADH vasoconstrict afferent more than efferent to decrease glomerular volume (glomerular pressure decreases  increased equilibration time  more filtration occur)  more Na+ out of tubule and therefore increase drive for moving water out of tubule (following Na+) Vasoconstricting afferent more than efferent also decreases flow in vasa recta therefore increasing equilibration time to uptake more water so that blood leaves less concentrated. Therefore, because removing less solutes from ISS and ISS gets concentrated and therefore increase drive for water movement even more. FALL 2004 7. Diagram and describe the events of the cardiac cycle of the left ventricle through diastole and systole showing the relationship between ventricular pressure and ventricular volume. Indicate the changes that would occur in this relationship with an increase in end diastolic volume and describe why these changes would occur Answer: 1) Diastole – ventricular relaxation during which filling occurs (volume increases but pressure stays the same) 2) Atrial contraction – during diastole of ventricle causing P wave in ECG reading (volume increases and pressure increases) 3) Isometric contraction – Because P ventricle is greater than P atrium, mitral valve closes. Aortic valve closes because Pressure in Aorta is still greater than the pressure in ventricle. Therefore, no volume coming in or out (no change) but contraction occurring (pressure increases) 4) Blood ejected from heart (once Ventricular pressure reaches 80mmHg, Aortic valve opens up because P ventricle is greater than P aorta, releasing blood from ventricle) Aortic pressure goes up to 120mmHg 5) Aortic blood volume increases  Aortic blood pressure increases 6) Ventricular relaxation 7) P ventricle < P aorta  Aortic valve closes (no volume change, but still relaxing  isometric relaxation) 8) P ventricle drops and eventually Mitral valve opens because P ventricle < P atrium 9) Rapid filling occurs and goes back to another cycle Increased end diastolic volume results in storing blood in the left ventricle which then increase the size of heart. According to the Frank Starling law of the heart, heart increases its contractility if EDV increases. As shown in Tension length relationship in skeletal muscle, actin-myosin length increases as volume increases. As it increases, the a-m length becomes close to optimal length for them to interact, and therefore cause contraction in cardiac muscle as well. But once it reaches the optimal length, the force generated (in cardiac muscle, contractility) decreases, because it gets harder for actin and myosin to interact. Physiologically it is impossible because unlike skeletal muscle, cardiac muscle is wrapped around by pericardium which sets limit for heart to expand. 2 Therefore in response to increased end diastolic volume, the heart increases its contractility and therefore increases stroke volume to compensate the change. Diagram) 8. Diagram the action potential of a cell in the SA node and describe the changes in Vm and channels involved in establishing this action potential. Indicate where the refractory periods occur. What is the role of refractory periods in the cells of the heart and describe why they are necessary for proper heart contraction Answer: 1) Resting potential of SA node is higher than other cells, so that they can spontaneously depolarize. Resting Vm = -70mV 2) Na+ slow flux in via Na+ leaky channel so Vm can reach threshold. The heart rate greatly depends on the length of Na+ flux aka IF 3) When it reaches the threshold, voltage gated L type Ca2+ channel opens causing Ca2+ flux in. This Ca2+ channel is slower compared to Na+ channel found in skeletal muscle. But both have open  inactive  close states. (depolarization) 4) Ca2+ channels get inactivated stopping Ca2+ fluxing in 5) K+ channel opens and start to repolarize the cell membrane 6) Ca2+ channels close so that it can be reopened for the next cycle 7) K+ channel closes In action potential of SA node, there are three different refractory period. Effective refractory period starts when V-gated Ca2+ channel opens and ends when V- gated Ca2+ channel close. Because it is not a set period of time, it’s not absolute refractory period. (when HR goes up, the whole events occur faster) During effective refractory period, another AP cannot be generated even in presence of greater stimulus. Relative refractory period starts when Ca2+ channel closes and ends when K+ channel closes. During relative refractory period, another AP can be generated if greater stimulus is given. Physiologically it’s not possible, because SA node generates its own AP via spontaneous depolarization. So in order to give greater stimulus, you can use defibrillator or any external stimuli. After K+ channel closes, there is a period when you can generate the AP with sufficient magnitude of Vm change. Because Ca2+ channel is still closing (slow), it cannot have Ca2+ flux into the cell; therefore you cannot have full excitation of membrane. This period is called post repolarization refractory period. Once Ca2+ channels are all closed, you can generate another AP and another cycle starts. Diagram) 9. You are on the way to the Keg after your physiology test and sadly you fall, hit your head and are losing blood. Explain how a loss of 500ml of blood volume would immediately affect fluid flux across one of your skeletal muscle capillary beds. Describe how the release of ADH-VP would be affected as a result of the fluid fluxes your just described. Answer: Loss of 500ml of blood volume results in decrease in volume in skeletal muscle capillary beds. Since volume and pressure is associated, pressure in cap bed also decreases. Because ∆P = Pc – Pt, ∆P decreases. There is no change is osmotic pressure so stays the same; therefore ∆ stays the same. This change will cause more reabsorption to occur (tissue  cap) and less filtration to occur (cap  tissue). Since osmolarity of the blood is mainly due to plasma protein (20mmHg > 5mmHg from electrolyte), and cannot move plasma protein because it’s too big to move through the membrane, you are only moving water and electrolyte across the membrane. Overall you have diluted blood in greater volume. There are two sensors for ADH VP release, which are high& low baro Rc (hemodynamic stimulus) and osmo Rc in hypothalamus(osmotic regulation). Volume increase causes decreased ADH release via high and low Baro Rc stimulation. Baro Rc sends information to brain stem and then to hypothalamus. Hypothalamus then decreases activity of ADH secreting cells so that ADH release will decrease. Also Osmo Rc in hypothalamus senses the change in blood osmolality by shrinking and swelling. By changing AP frequency of neurons that release ADH, it decreases in response to decreased osmolality. Compared to hemodynamic stimulus, osmo stimulus has greater impact on ADH release. Overall, you have decreased ADH level. 10. Blood loss can stimulate the release of renin. Describe how an increase in blood levels of renin would affect the production of other hormones and describe their effects on the kidney and its associated vasculature to alter water loss at the kidney Answer: Renin is released in response to various stimuli. When afferent arteriole pressure (or volume) increases, and when NaCl in macula densa increases, renin secretion decreases (local control). Centrally increase SNS activity on afferent and efferent (via direct innervation), increases the release of renin (central control). Renin in blood helps angiotensinogen (synthesized in the liver, circulating, inactive) to convert to Angiotensin I. From endothelial cell of kidney afferent arteriole or lung, angiotensin converting enzyme is released, making AI to AII. It works on adrenal gland to increase aldosterone release. A II works locally to increase resistance of efferent to decrease renal blood flow so that GFR will increase (more filtration time). Centrally, A II increases ADH VP release from post pituitary gland to insert more water channels at distal tubule and collecting duct to increase water permeability. Aldosterone increase Na+ reabsorption in late DT and CD and water follows the Na+ (therefore more water moves to peritubular capillary) 11. Tachycardia can result from an increase in SNS activity to nodal cells of the heart. Describe how a change in resting heart rate to 150bpm would affect pressure in the aorta and how this change in pressure would immediately affect fluid flux across one of your skeletal muscle capillary beds. If the tachycardia changed resting heart rate to 250bpm, describe how this change in heart rate would affect pressure in the aorta and why. Describe how this change in pressure would affect fluid flux across the same capillary bed? Answer: Tachycardia is characterized by abnormally fast heart beat. Direct innvervation SNS releases norepinephrine to SA node, and this increases the Na+ leak rate so that time to reach threshold will be decreased. This results in increased spontaneous depolarization rates and increased heart rate. If heart rate is changed to 150 bpm, end systolic volume decreases because of treppe phenomenon. As heart rate increases, phosphorylation of L type Ca2+ channel occurs faster allowing more Ca2+ influx to the cell (trigger Ca2+), therefore increased contractile force, increased stroke volume and decreased end systolic volume. This results in increased blood volume in aorta, and increased aortic pressure. 3 In skeletal muscle capillary bed, there will be increase in MAP but no change in MCFP. There will be increased volume coming in, and same amount of blood going out. As a result, you will have more blood in cap bed; therefore increased pressure. ∆P = P capillary – P tissue, so ∆P also increases but no change in ∆. There will be more filtration occurring (cap  tissue), and less reabsorption occurring (tissue  cap). Overall, increased fluid flux from capillary bed to tissue would occur. If resting heart rate becomes 250 bpm, the stroke volume decreases. There are 3 basic ways that heart rate controls stroke volume. After 180 bpm, negative effect outweighs positive effect. Because increased heart rate also means, decreased duration of events including duration of diastole where ventricular filling occurs. There will be less end diastolic volume due to decreased filling time, therefore the stroke volume would decrease (so does Cardiac output). Since the cardiac output decreases, there will be less volume and pressure in aorta. Decreased MAP with the same MCFP, you will have less blood in capillary bed therefore decreased ∆ P with constant ∆ . Less filtration (cap  tissue) occurs while reabsorption(tissue cap) increases. Overall there will be increase in fluid flux to capillary. 12. Dehydration causes a decrease in blood volume and an increase in plasma protein concentration. Describe how dehydration would affect the release of renin Answer: Dehydration results in increased ∆  and decreased ∆ P. Therefore more fluid flux will occur from tissue to capillaries. Renin release is controlled both locally and centrally. Perfusion pressure which is pressure in afferent arteriole and NaCl in macular densa are inversely proportional to renin release while SNS activity on afferent and efferent arterioles are directly proportional to Renin release. Decreased blood volume is detected by low pressure (at right atrium and pulmonary artery) and high pressure baro Rc (carotid artery and aorta) detects the change and stimulates SNS activity to acts on various vascular smooth muscle to increase blood volume. And as SNS activity increases renin release increases as well. As blood volume decreases, afferent arteriole pressure decreases and therefore renin release increases. Also blood volume decrease causes less blood flowing into the glomerulus therefore less pressure, and less glomerular filtration rate (more equilibration time). Na+ reabsorption is increased, and there will be less Na+ detected in macular densa therefore renin release is increased. FALL 2005 13. Graph the intrinsic relationship between end diastolic volume and stroke volume produced by the heart ventricles. Explain why this occurs and discuss its physiological relevance. How is the upper limit of this relationship set? Answer: end diastolic volume is also known as preload and increased EDV is coupled with increased contractility. According to the Frank Starling law of the heart, heart increases its contractility if EDV increases. As shown in Tension length relationship in skeletal muscle, actin-myosin length increases as volume increases. As it increases, the a-m length becomes close to optimal length for them to interact, and therefore cause contraction in cardiac muscle as well. But once it reaches the optimal length, the force generated (in cardiac muscle, contractility) decreases, because it gets harder for actin and myosin to interact. Physiologically it is impossible because unlike skeletal muscle, cardiac muscle is wrapped around by pericardium which sets limit for heart to expand. Therefore in response to increased end diastolic volume, the heart increases its contractility and therefore increases stro
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