Lesson 15, 16, and 17. Regulation of the Cardiovascular System. 1. Arteriolar resistance helps provide constant flow despite changes in perfusion pressure. The depolarization of smooth muscles increases the frequency of spike discharge which leads to increased contractions. How can distention promote smooth muscle repolarization? a. Stretch-sensitive cationic channels b. Cl- channels c. Rise in perfusion pressure and increased flow d. All of the above 1. D: A rise in perfusion pressure and increased flow initially pushed on stretchsenstivie cationic or Cl- channels and leads to narrowing of the vessel which increases resistance and allows flow to return to constant state. Less area at the same velocity (P=A*V) causes a decrease in pressure. This decrease in pressure removes activation of stretch-sensitive cationic channels and thus lowers membrane potential -> lowers probability of spike discharge -> relaxes smooth muscle and increases area -> resistance falls and flow goes back up.
2. What statement best explains this figure:
a. Dotted line is the steady state flow at a new perfusion pressure b. Dotted line is the flow after abrupt changes in perfusion pressure c. Solid line is the steady state flow at a new perfusion pressure d. b & c
2. D: The myogenic response initially allows flow to increase with high perfusion pressure then it regulates it back to normal.
3. During exercise, blood flow is initially not enough to meet the tissue demands. Because of this: pO2 falls and pCO2/H+ rise to vasodilate -> reduce resistance -> increase flow. High K+ and osmolality in blood also increase flow. Adenosine is another vasodilator of heart and skeletal muscle. Whats true about adenosine? a. made with a 5’ GMP precursor b. made with a reaction using myokinase c. can alone account for changes in blood flow d. uses 5’-Kinase 3. B: Adenosine is made with 2 ADP + myokinase that makes 5’ AMP which 5’ nucleotidase uses to make adenosine.
4. Which of the following do not vasodilator or decrease smooth muscle tone? a. Adenosine b. High ExCellular K+, H+, Osmolarity, or Pi c. Low pO2 d. High pCO2, shear stress, or NO e. Distention
4. E: Adenosine, high K,H,Osmol,Pi,pCo2, shear stress, NO and low pO2 will vasodilate. Distention causes contraction.
5. What is not a mechanism for vasodilation? a. Activation of myosin light chain kinase (MLCK) b. Inactivation of myosin light chain kinase (MLCK) c. Reduced intracellular mobilization of Ca2+ d. Hyperpolarization of smooth muscle
5. A: Vasodilation can occur via inactivating MLCK, reducing intracellular Ca2+, or hyper polarizing smooth muscle.
6. Which description does not accurately describe how smooth muscle cells vasodilate? a. Hyper polarize with K+: Katp/Kir/BKca channels hyper polarize the smooth muscle cell due to H+, pCO2, K+, and EDRF NO extracellular increase. b. Reduce Ca: NO cascade decreases Ca conductance and increases Ca resequesering. Shear stress and low pCO2 -> + NO -> less Ca inside. c. Inhibit MLCK which usually helps smooth muscles contract: Adenosine -> Adenylate cyclase activation -> cAMP -> PKA -> Inhibit MLCK d. Reduce Ca: Adenosine -> Adenylate cyclase activation -> cAMP -> PKA -> Inhibit MLCK 6. D: Super easy but don't want to mix up too much because it’ll be easily confused. A, B, and C are true. D is just a bad combo and makes no sense :). Not a tough q but good repetition.
7. Neural and humoral extrinsic systems help provide a specific increased flow to one place and lowered flow to another to redistribute in stressful situations. What is not true about neural regulation of resistance (arteries) vessels? a. Sympathetic system releases NE that binds a-1 receptors to control S.M. of ateries/ arterioles to control total peripheral resistance (has basal tone) b. Sympathetic cholinergic vasodilator fiber only discharge during exercise and defense and is mediated by NO/Ach. c. Parasympathetic cholinergic vasodilatory fiber in glands released kallikrein -> bradykinin -> NO. Only in few tissues. d. Parasympathetic cholinergic vasodilatory fiber modulates all of vascular resistance by increasing or decreasing firing.
7. D: Sympathetic cholinergic vasodilatory fiber modulates all of vascular resistance by increasing or decreasing firing. Rest is true!
8. What is true about neural regulation of capacitance (veins) vessels? a. Sympathetic vasoconstrictor nerves release NE through a-1R to activate vein constriction (sparsley) b. Venous capacitance can be controlled through sympathetic discharge c. Contraction reduces compliance, pushed blood to heart, and raises arterial blood pressure d. Parasympathetic nervous system regulates venous tone 8. All are true but PS DOES NOT regulate venous tone
9. Parasympathetic and sympathetic ANS regulate cardiac function. Vagus nerve provides PS innervation (SA is right vagus, AV is left vagus) as well as atria and ventricles. Vagal and Symp are tonic. At rest, PS tone dominates. How does the mechanism of antagonism work between the two? a. Ach is released from vagus nerve and interacts with AchR on sympathetic nerves to inhibit NE release b. Ach is released from symp nerve and interacts with AchR on vagus nerves to inhibit NE release c. Ach is released from symp nerve and interacts with AchR on heart to lower HR d. Ach is released from vagus nerve and interacts with AchR on heart to lower HR 9. A: Ach is released from vagus nerve and interacts with AchR on sympathetic nerves to inhibit NE release
10. The central cardiovascular control center exists in the medulla oblongata and pons. What is not true about this area? a. Spontaneously active pressor area autonomic motor neurons excite preganglionic sympathetic neurons in spinal cord. b. The sympathetic neurons of the depressor area do the opposite of the pressor area. c. Parasympathetic neurons are not spontaneously active but they have a tonic inhibitory influence on the heart due to input from arterial stretch receptors. d. Parasympathetic neurons are spontaneously active and they have a tonic inhibitory influence on the heart due to input from arterial stretch receptors.
10. D: All are true except D.
11. What is true about arterial baroreceptors? I. Found in adventitia II. Carotid sinus use glossopharyngeal nerve & aortic arch travel use depressor/aortic/ buffer nerve III. Firing caused by instanenous pressure + rate of change of pressure IV. Firing rises with increased pulse pressure even if MAP is same V. Decrease in Stroke volume -> Decrease in pulse pressure (no decrease in MAP) -> Communicated to center a. I & II b. I, II, & III c. I, II, III, & IV d. I, II, III, IV, & V
11. All are true.
12. What best explains this graph of MAP and baroreceptor activity?
a. Sinus nerve fires are lower threshold than aortic nerve b. Aortic nerve fires are lower threshold than sinus nerve c. Greater change in MAP is required to change baroreceptor firing for aortic nerve d. Greater change in MAP is required to change baroreceptor firing for sinus nerve e. a & c f. b & d 12. E: Aortic nerve has higher threshold before it fires. It aortic baroreceptors don’t change in fire rate as much due to increase in MAP (slope shows “buffering” effect). These baroreceptors synapse in the Nucleus Tracts Solitarius (NTS) that activate the cardioinhibitory depressor area which inhibit the pressor and pregang.sympathetic neurons of spinal cord.
13. Baroreceptors synapse in the Nucleus Tracts Solitarius (NTS) that activate the cardioinhibitory depressor area which inhibit the pressor and pregang.sympathetic neurons of spinal cord. When MAP falls and baroreceptors aren't activated, the pressor area is disinhibited causing excitation of sympathetic. What is true about this diagram? NTS: Nucleus Tractus Solitarius X: Vagal Nerve 10 D: Depressor P: Pressor PrGSN: Pregranglionic Sympathetic neuron
a. Active NTS activates X and D b. Active NTS inhibits X and D c. P inhibits PrGSN d. NTS activates PrGSN 13. A: Active NTS activates X and D. P uncontrolled will activate PrGSN. NTS will end up inhibiting PrGSN through activating D.
14. Dishinihibtion of pressor area and activation of preganglionic sympathetic neurons leads to: a. Increase in total peripheral resistance b. Increased Venous tone c. Increased HR d. Increased constriction of arterioles and small arteries (except in heart or brain) e. All of the above 14. E: All are true. Sym causes high TPR, high contractility, high HR, high constriction in kidney/skelt muscles but not heart/brain, and high venous tone.
15. What are the components of the reservoir model? a. Aorta; reservoir (pgh) b. TPR in arterioles: cup where fluid pours in c. Highly compliment veins: reservoir (pgh) d. Heart; Narrowing of tube 15. A is correct; TPR in arterioles rep by narrowing. Veins rep by last segment of tube. Heart rep by cup where fluid pours in.
16. What is now true about the filling of the cup of the reservoir? a. End Systolic Volume ESV is the stored volume b. End Diastolic Volume EDV is the max filled (“dilled�) volume c. Stroke volume is the difference between the EDV and ESV or the volume that had left the reservoir or the volume that refilled the reservoir d. SV is equal to what is collected between a beat and must be equal to the reservoir runoff between beats e. All of the above
16. E: All are true
The highest level of fluid 120mmHg is the systolic pressure. After the loss of this fluid, the remaining pressure of 80mmHg is the diastolic pressure. If the volume drained is 100ml w/ a HR of 60bpm (1 b per sec): 100 ml are drained per second. That means in a second 100ml must also flow back to the heart to return to the original systolic value of 120mmHg. Because fluid and thus pressure is lost over time, the rate of runoff steadily decreases as volume is lost. That means more than half the 100ml volume is lost in the first 1/2s and less than 50% of the volume is lost in the second 1/2 s.
17. What does not happen if the diameter for the TPR part is narrowed? a. Resistance increases b. Flow is slower c. EDV is lower in cup but EDP is higher in reservoir (less volume leaves the reservoir) d. Stroke volume is higher (starling relates EDV to SV) 17. D: Stroke volume decreases as EDV decreases. The result is that EDV in the heart (cup) will be lower than normal just before the next beat, and diastolic pressure in the reservoir will be higher. High TPR = Low Flow = Low CO/VR = High MAP (due to higher diastolic PRESSURE). An increase in resistance and therefor more fluid stored in reservoir causes EDP to be higher. With a decrease in resistance, Map will be low and flow will be high.
18. When veins are constricted, the rise in venous resistance increases the amount of fluid in the reservoir thus increasing the EDV (and therefore SV). More than 100 ml is returned and the systolic pressure will also rise. This is how veins cause a net transfer of fluid to the reservoir. What will happen to systolic pressures? a. Not enough time to fill fluid so diastolic pressure is increased along with systolic pressure b. MAP increases but TPR increases only a bit so flow is increased c. Reservoir aortic pressure and flow (CO & VR) have increased d. All of the above 18. Venous constriction increased MAP and TPR (a bit) which increases flow (CO/VR), but not enough time to refill so diastolic pressure increased as will as systolic. AN increase in venous compliance (less venous tone) will decrease MAP and decrease flow (CO/VR). The extra fluid comes from the veins.
19. What are the consequences of a decrease in contractility? a. force of cardiac contraction greater than normal b. stroke volume greater than normal c. ESV stores are now expelled d. Diastolic and systolic pressures decrease 19. D: Diastolic and systolic pressures decrease with decreased contractility. Furthermore, cardiac contraction/SV is less, ESV is not used and some EDV is left over.
20. An increase in HR from 60bpm to 120bpm reduces time for run off and less blood leaves so diastolic pressure is higher. Less EDV is needed to refill and so the SV is also less. Every 1/2 second the 120mmHg systolic pressure is returned. High diastolic pressure increases MAP and flow increases also. Doubling the heart rate in the scenario will increase cardiac output (HR (60 -> 120) xSV(100ml -> 50ml) =CO (61 -> +61). What would occur if the heart rate was halved to the diastolic pressure, MAP, flow, EDV, and SV? a. Diastolic pressure decreases, MAP decreases, flow decreases, EDV increases, SV increases b. Diastolic pressure decreases, MAP decreases, flow increases
increases, EDV increases, SV
c. Diastolic pressure increases, MAP decreases, flow decreases, EDV increases, SV increases d. Diastolic pressure increases, MAP decreases, flow increases, EDV increases, SV increases
20. A: In decreasing HR, the diastolic pressure decreases, MAP decreases, flow decreases, EDV increases, and SV increases
21. What factors increase MAP? a. Decreased TPR(-CO),Increased Contractility(+CO), Increased Heart Rate(+CO), Decreased Cv(+CO) b. Increased TPR(-CO), Increased Contractility(+CO), Increased Heart Rate(+CO), Decreased Cv(+CO) c. Decreased TPR(-CO), Decreased Contractility(+CO), Increased Heart Rate(+CO), Decreased Cv(+CO) d. Decreased TPR(-CO), Decreased Contractility(+CO), Decreased Heart Rate(+CO), Decreased Cv(+CO) 21. B: Increased TPR(-CO), Increased Contractility(+CO), Increased Heart Rate(+CO), Decreased Cv(+CO)
22. What factors decrease MAP? a. Decreased TPR, Decreased Contractility, Decreased Heart Rate, Increased Cv b. Increased TPR, Decreased Contractility, Decreased Heart Rate, Increased Cv c. Increased TPR, Increased Contractility, Decreased Heart Rate, Increased Cv d. Increased TPR, Increased Contractility, Increased Heart Rate, Increased Cv 22. A: Decrease in MAP is correlated with low TPR, contractility, HR, and high Cv (venous compliance)
23. Single stretch receptors in the carotid sinus discharge at frequencies dependent upon the arterial pressure. At low arterial pressure the lack of firing of baroreceptors has the cardiovascular control center (CVCC) responds by decreasing vagal nerve impulse frequency and by increasing sympathetic cardiac nerve impulse frequency so that HR and contractility rise to increase blood pressure. What best explains this chart?
a. At low arterial pressure sympathetic vasoconstrictor nerves fire less b. At low arterial pressure vagus and carotid sinus nerves fire more c. At high arterial pressure vagus and carotid sinus nerves fire less d. At high arterial pressure sympathetic vasoconstrictor nerves fire less
23. D: At high arterial pressure sympathetic vasoconstrictor nerves fire less because the pressor are inhibited.
24.Reflex dilation occurs when the forearm blood flow increased due to raising of the legs in anticipation (as compared to if just cuffed) because it is caused by displacement of blood. What is the feed-forward reflex? a. When EDV increases; non-myelinated vagal nerves increase firing due to dissension and total peripheral resistance is lowered b. Cardiac output is matched by outflow in arteries and arterial blood pressure is not altered c. Non-Myelinated vagal fibers in atria/ventricles induce depressor response upon firing due to distention and pressor response upon lack of firing d. Non-Myelinated vagal fibers in atria/ventricles induce pressor response upon firing due to distention and depressor response upon lack of firing
24. C: A and B are true but C is the definition of the feed-forward reflex.
25. Myelinated vagal fibers fire due to stretch of atrial junction receptors to imitation a selective reflex that only raises heart rate (not contractility). The bainbridge response: a. Ensures a larger VR is converted to CO through an increase in HR b. Ensures a larger VR is converted to CO through an decrease in HR c. Ensures a smaller VR is converted to CO through an increase in HR d. Ensures a smaller VR is converted to CO through an decrease in HR 25. A: Bainbridge response of atrial junction ensures a larger VR is converted to CO through an increase in HR. It dominates over unmyelinated response in increasing HR.
26. What is not true about epinephrine?
a. Released from adrenal medullary chromaffin cells b. Released when blood pressure increases (a1 constrict due to NE firing) or exercise/ fear (BR relax) c. B-receptor mediates increase in HR, Contractility, and a-1R venous tone d. a-1R response in kidneys/mesentery mediates contraction and B-R response in arteries dilated smooth muscle e. At low concentrations BR causes dilation + and high concentration a-1R causes constriction
26.B: Epinephrine (adrenal medulla chromaffin): blood pressure decreases (a1R constricts) or exercise/fear (BR relax). B1R cares for increasing HR and contractility. A1R cares for increases venous tone (decrease venous complaince). A1R in kidneys/ mesentery so contraction. BR in arteries so dilation. Low concentrations more BR so dilation. In high concentration more A1R so constriction.
27. Juxtaglomerular kidney cells release renin protease due to sympathetic impulse. It cleaves angitensinogen to form angiotensin I (10 peps). Angiotensin converting enzyme (ACE) in lungs then cleaves it to form angiotensin II (8 peps). What is true regarding AII functions? I. Affects arterioles and sympathetic activity norepinephrine release II. Enhances depressor response for short term BP effects III. Controls secretion of aldosterone and ADH release (no pee hormone) IV. Controls body water via kidney Na reabsorption a. I b. 1, II, IV c. I, III, IV d. I, II, III, IV 27. C: AII enhances pressor not depressor response. It also increases NE, aldosterone, and ADH release (which controls Na reabsorption).
28. An INCREASE in tissue fluid or decrease in blood volume/pressure causes the release of antidiuretic hormone due to reduced pressure of baroreceptors. ADH (vasporessin) reabsorbs H2O back into the blood stream. What is true about both ADH and AII? a. hypotension activates both neural and hormonal triggers for ADH secretion. b. If the concentrations are higher than needed, it will cause constriction in all tissues except for the heart and brain. c. Short term effect is vasoconstriction and long term effect is increasing plasma volume via kidney salt intake d. All of the above 28. C: C is true for both. A and B is just referring to ADH.
29. Atrial natriuretic peptide is made by mycoses in the atria. It is released by dissension due to high blood volume. It acts in an opposing was to AII. What is incorrect about ANP? a. Directly relax kidney arterioles + lower total peripheral resistance b. Inhibits pressor area + Ach release of sympathetic nerves c. Inhibits renin synthesis, promotes water/salt loss d. All are true 29. D: ANP does a lot! It does the opposite of AII and more!
30. What does the hypothalamus do? a. Vasodilation of cutaneous and vasoconstriction of viscera + raise BP in fear response via vasoconstriction, high contractility, high venous tone b. Selective dilation of skeletal muscle via increasing inhibition of symp nerves, increase in epinephrine B-2R dilation, increase in symp skel impulse c. Inhibit solitary tract nuelcues so less responsive to baroreceptors (ie usually dampened in excersise to HR/Contractility don't decrease) d. All of the above 30. D: All of the above again! The hypothalamus defense response: increases muscle artery dilation, increases skin vasodilation/sweating, increases epinephrine B-2 muscle dilation via blood stream, reduces vagal fibers and increases NE to raise HR/ Contractility, increase venous constriction, increase sympathetics to kidney/ mesentary. Cerebral cortex monitors the psychogenic response of fainting via bradycardia and vasodilation from vagal outflow and sympathetic suppression.
31. Using the graph below, select all possible long term effects on the regulation of circulation:
I. Redistribute existing blood volume II. Capillary fluid shifts due to hydrostatic pressure III. Angiotensin stimulus thirst, aldosterone (Na reabsorption), ADH (water reabsorption; released due to low baroreceptors) IV. ANF vary opposing angiotensin V. Kidney function greater urine output at high renal arterial pressure (pushes water to tubules) a. I, II, III b. I, II, III, IV c. II, III, IV, V d. I, III, IV, V
31. C: I is for short term effect. Long term effects shift create new standards for blood volume.