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Flashcards in Autonomic Control of Blood Pressure Deck (31)
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what is the single most important mechanism providing short-term regulation of arterial pressure?

the arterial baroreceptor, most importantly high-pressure carotid sinus, then aortic arch


how is MAP monitored?

1. high-pressure arterial baroreceptors (on arterial side, most importantly carotid sinus then aortic arch)
2. renal juxtaglomerular apparatus
3. low-pressure baroreceptors (AKA volume or cardiopulmonary receptors, on venous side and atrium)
4. chemoreceptors (although mostly for respiratory control)


how are adjustments to MAP made?

via the ANS and release of specific hormones


where do all baroreceptors feed back to?

the nucleus tractus solitarius (NTS) in medulla


where do carotid baroreceptors feed back to?

from carotid sinus; transmitted thru Hering's nerve to CN IX in high neck, then to NTS


where do aortic baroreceptors feed back to?

from aortic arch; transmitted thru CN X to NTS


what happens if there is stretching of distensible vessel walls at the high-pressure baroreceptors?

stretching at carotid sinus and oartic arch causes reflex vasodilation and bradycardia


peripheral chemoreceptors

located in carotid and aortic bodies, and in close contact with arterial blood
-when arterial pressure falls below a critical level, the receptors are stimulated b/c less blood flow causes less O2
-signals transmitted from chemoreceptors and baroreceptors pass thru Hering's and IX nerves (if carotid) and vagus (if aortic) to NTS to elevate MAP back to normal


is the chemoreceptor reflex a powerful MAP controller?

not until MAP falls below 80 mmHg (like during hemorrhage)
-thus it's at lower pressures that this reflex becomes important to prevent further decreases in MAP


central chemoreceptors

in the medulla
-sensitive to decreases in brain pH reflecting increase in arterial PCO2
-causes increase in SNS output


what do low PO2 and high PCO2 act on, what what is their effect?

low PO2 acts on peripheral chemoreceptors, and high PCO2 acts on central chemoreceptor
-they act in concert to enhance vasoconstriction


low-pressure baroreceptors

in cardiovascular system
-detect changes in venous pressure/volu


what happens to baroreceptor APs and receptor potentials in response to higher pressure?

higher pressure (steps) --> higher receptor potential (depolarization) --> more frequent APs


structure of baroreceptors in carotid sinus and aortic arch, and what are they sensitive to?

branched terminals of myelinated and unmyelinated sensory nerve fibers, intermeshed within elastic layers
-they are sensitive to stretch


what does an increase in transmural pressure difference do?

enlarges the vessel, deforming the receptors, and increasing firing rate of the baroreceptor's sensory nerve
-the signal is frequency modulated


to what do baroreceptors respond to, and when are they most sensitive?

they respond rapidly to changes in MAP and are most sensitive in normal operating range ~100 mmHg for carotid sinus, and 130 mmHg for aortic arch (less sensitive)
-the slope of dI/dP is maximum at this time


when do carotid sinus baroreceptors not work?

they are not stimulated by pressures between 0 to 50 or 60 mmHg
-above these levels, they respond progressively more rapidly and reach a maximum at 180 mmHg, and are optimal at 100 mmHg


what happens to the rate of impulse firing during systole and diastole?

the rate increases in the fraction of a second during each systole, and decreases again during diastole


do baroreceptors respond more to rapidly changing pressures or stationary pressures?

they respond more to rapidly changing pressures
-ex: if MAP is 150 mmHg, but is rising rapidly, the rate of impulse transmission may be twice that when the pressure is stationary at 150 mmHg


what happens to the baroreceptor reflex in HTN?

since it adapts to long-term changes in MAP, the curve is parallel and shifts to right (meaning it's not as sensitive)


what would happen to MAP if baroreceptors were absent?

MAP would fluctuate wildly if the baroreceptors were denervated, and no longer be constantly monitored
-the MAP would have a very wide range, instead of the usual ~100mmHg


what is the primary purpose of arterial baroreceptor system?

reduce the minute-by-minute variation in arterial pressure to about one-third that which would occur if the baroreceptor system was not present


in general, how many vessels does the SNS innervate? what does this mean?

in most tissues they innervate all vessels except capillaries
-precapillary spinchters and metarterials are innervated in some, but not as densely
-innervation of small arteries/arterioles allows SNS stimulation to increase R and decrease Q
-innervation of large vessels, especially veins, allows SNS to vasoconstrict to push blood into heart to regulate CO (decrease compliance of vessels)


what does the vasoconstrictor area of the vasomotor center do?

it transmits signals continuously to the sympathetic vasoconstrictor nerve fibers over the entire body
-causes slow firing of these fibers at a rate of about 1/2 to 2 impulses per second
-these impulses normally maintain a partial state of contraction in blood vessels, called vasomotor tone


what does total spinal anesthesia do? and how can it be reversed?

it blocks all transmission of sympathetic nerve impulses from the spinal cord to the periphery
-thus, the MAP falls from 100 to 50 mmHg, demonstrating the effect of losing vasoconstrictor tone throughout the body
-it can be reversed by injecting NE so vessels constrict and MAP rises to an even greater level (~140 mmHg, for several minutes) until the NE is metabolized, and MAP decreases again


what does an increase in MAP cause?

activates negative feedback via high-pressure baroreceptors (detector)
-go via their afferent pathways to coordinating center (NTS in medulla)
-efferent pathways cause vasodilation of veins/arterioles thru peripheral circulatory system, and decreased HR and strength of contraction
-bradycardia and vasodilation will decrease MAP


what happens when one changes posture from standing to lying down?

there is an increase in (central) venous return and SV, which leads to an increase in MAP
-increases firing rate of baroreceptor afferent fibers, which feed back to NTS in medulla
-effectors increase PNS and decrease SNS, which feed back to SA node
-work together to decreases HR and CO (thus decrease SV)
-SNS decreases peripheral resistance in arterioles, decrease venous tone in veins, and decrease contractility in ventricles to decrease SV and CO
-altogether, will decrease MAP


what happens when one stands up from lying down?

pooling of blood in veins will decrease arteriolar pressure
-the baroreceptor fires less, thus causing and increase in sympathetic outflow (increased HR, contractility, CO, arterolar and vein constriction to increase TPR
-minimizes the decrease in pressure in head and upper body


what does the carotid sinus massage, or release from a Valsalva maneuver do?

stimulates the baroreceptors and reflexly slows heart in people with atrial tachycardia (atria flutter or fibrillation) to decrease HR


carotid sinus syndrome

patients have hyper-sensitive baroreceptors such that even mild external pressure to the neck causes a strong reflex, and may even stop the heart for 5-10 seconds (syncope)

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