scholarly journals Aortic Baroreceptors Display Higher Mechanosensitivity than Carotid Baroreceptors

2016 ◽  
Vol 7 ◽  
Author(s):  
Eva On-Chai Lau ◽  
Chun-Yin Lo ◽  
Yifei Yao ◽  
Arthur Fuk-Tat Mak ◽  
Liwen Jiang ◽  
...  
Keyword(s):  
Carotid Baroreceptors ◽  
Aortic Baroreceptors

Effect of carotid or aortic baroreceptor denervation on arterial pressure during hemorrhage in conscious dogs

2001 ◽  
Vol 280 (6) ◽  
pp. R1642-R1649 ◽  
Author(s):  
Terry N. Thrasher ◽  
Cassandra Shifflett
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Conscious Dogs ◽  
Carotid Baroreceptors ◽  
Intact Condition ◽  
Aortic Baroreceptors

We studied the effect of chronically denervating aortic baroreceptors (ABR; n = 6) or carotid baroreceptors (CBR; n= 7) on mean arterial pressure (MAP) and heart rate (HR) responses to hemorrhage in the dog. Neither denervation had a significant effect on basal MAP, the variability (standard deviation) of MAP, or resting HR. However, the breakpoint of MAP (defined as the volume of blood removed when MAP fell more than 10% below control and declined monotonically thereafter) was significantly reduced in dogs with only ABR functional (12.4 ± 1.4 ml/kg) compared with the volume in the intact condition (18.9 ± 1.8 ml/kg). In contrast, there was no difference in the breakpoint or the MAP at any time during hemorrhage in dogs with both CBR functional compared with their intact responses. In a different group of dogs ( n = 6), responses were determined with both CBR operating and again after unilateral denervation, leaving only one CBR (1CBR) functional. Basal MAP and the variability of MAP were not altered in dogs with only 1CBR functional, but the breakpoint (11.7 ± 1.4 ml/kg) during hemorrhage was significantly different compared with responses with two CBR (21.2 ± 2.3 ml/kg), and MAP fell to much lower levels. These results indicate that the CBR can compensate fully for loss of ABR during hemorrhage but not vice versa; and bilateral CBR inputs are required for normal responses to hemorrhage.

Baroreceptor output during normal and obstructed breathing and Mueller maneuvers

1981 ◽  
Vol 240 (5) ◽  
pp. H721-H729 ◽  
Author(s):  
R. S. Fitzgerald ◽  
J. L. Robotham ◽  
A. Anand
Keyword(s):  
Blood Pressure ◽  
Systolic Pressure ◽  
Intrathoracic Pressure ◽  
Inspiratory Effort ◽  
Carotid Baroreceptors ◽  
Cardiac Responses ◽  
Inspiratory Phase ◽  
Mueller Maneuver ◽  
Aortic Baroreceptors ◽  
Anesthetized Cat

Cardiovascular control during asthma and other forms of obstructed breathing has not been extensively investigated. Previous studies in dogs have shown that obstructed breathing or an inspiratory effort against a blocked airway (Mueller maneuver) provoke large oscillations in blood pressure. During the inspiratory phase transmural systolic pressure relative to atmosphere drops initially, but transmural systolic pressure relative to intrathoracic pressure can remain unchanged or even increase. Because the carotid baroreceptors are located in the extrathoracic circulation, whereas the aortic baroreceptors are located in the intrathoracic circulation, and each responds to local transmural arterial pressure, simultaneous baroreceptor output from these two areas was measured in the anesthetized cat during normal and obstructed breathing and during Mueller maneuvers. Both whole-nerve and single-fiber preparations showed a significantly decreased output from the carotid baroreceptors during obstructed inspiratory efforts, whereas aortic baroreceptor output decreased significantly less or not at all. Transmural systolic pressure decreased significantly less in the aorta than in the carotid regions. Further, the aortic baroreceptors were more sensitive to changes in pulse pressure than were the carotid baroreceptors. These results suggest a mechanism for stabilizing the cardiac responses to precipitous falls in blood pressure that occur in obstructed breathing.

Carotid and aortic baroreceptor control of heart rate in conscious monkey

1987 ◽  
Vol 253 (4) ◽  
pp. H811-H817 ◽  
Author(s):  
M. W. Barazanji ◽  
K. G. Cornish
Keyword(s):  
Heart Rate ◽  
Aortic Arch ◽  
Carotid Sinus ◽  
Maximum Slope ◽  
Phenylephrine Hydrochloride ◽  
Carotid Baroreceptors ◽  
Arterial Blood ◽  
Significant Difference ◽  
The Difference ◽  
Aortic Baroreceptors

This study looks at the difference between the aortic and the carotid baroreceptors in controlling the heart rate of conscious monkeys in the cage vs. the laboratory. Macaca mulatta and M. radiata underwent sequential baroreceptor denervation by first stripping the aortic arch, then one carotid sinus, and finally the second carotid sinus [sinoaortic denervation (SAD)]. Four monkeys had the carotid sinuses denervated before denervation of the aortic arch. Mean arterial blood pressure (MABP)-heart rate (HR) curves were determined by infusing nitroprusside and phenylephrine hydrochloride. The peak sensitivity (PS) was significantly less for all animals (control and denervated) in the laboratory than in the cage (P less than 0.05) with the exception of the SAD animals, which showed no difference. There was no significant difference in sensitivity between control and aortic-denervated animals in the cage. The PS decreased significantly after denervation of aortic arch and one carotid sinus. Monkeys with only the aortic baroreceptors intact had gains for the baroreflex curves that were similar to that of the SAD animals. After complete SAD the PS were essentially zero. We concluded that 1) the maximum slope of the MABP-HR reflex is greater when the monkey is in the cage than it is in the laboratory, probably resulting from an increase in the sympathetic tone; and 2) the carotid baroreceptors exert a greater influence on the HR component of the baroreflex in the conscious monkey than do the aortic baroreceptors.

Differential baroreflex modulation of human vagal and sympathetic activity

1991 ◽  
Vol 260 (3) ◽  
pp. R635-R641 ◽  
Author(s):  
J. M. Fritsch ◽  
M. L. Smith ◽  
D. T. Simmons ◽  
D. L. Eckberg
Keyword(s):  
Sympathetic Activity ◽  
Peroneal Nerve ◽  
Pressure Step ◽  
Cardiac Responses ◽  
Baroreceptor Stimulation ◽  
Baseline Levels ◽  
Neck Pressure ◽  
Aortic Baroreceptors ◽  
Muscle Responses ◽  
Ambient Levels

We compared baroreflex modulation of human vagal-cardiac and sympathetic muscle activity in healthy volunteers by measuring R-R interval and peroneal nerve responses to a profile of positive and negative (40-65 mmHg) R-wave-triggered neck pressure steps during held expiration. R-R interval responses were sigmoid. Sympathetic activity increased abruptly with 40 mmHg pressure but returned to baseline levels as this pressure was maintained. The first decremental pressure step reduced sympathetic activity to below baseline, and the next three steps inhibited activity. During the final three steps, sympathetic activity increased to baseline, and after the return of neck pressure to ambient levels sympathetic activity increased to the highest levels recorded. Our results suggest that on a second-by-second basis human vagal-cardiac responses are determined simply by the net level of baroreceptor stimulation. Sympathetic muscle responses are determined complexly by the direction of changes (rising or falling) more than absolute arterial pressure levels and importantly by inputs from both carotid and aortic baroreceptors.

Flow and thermal responses of aortic baroreceptors

1993 ◽  
Vol 70 (6) ◽  
pp. 2596-2605 ◽  
Author(s):  
P. A. Munch
Keyword(s):  
Aortic Arch ◽  
Neural Control ◽  
Effect Of Temperature ◽  
Wide Range ◽  
Activation Response ◽  
Flow Through ◽  
Effects Of Temperature ◽  
Aortic Arch Pressure ◽  
Aortic Baroreceptors

1. The aims of this study were 1) to determine whether the impulse activity in rabbit aortic baroreceptors (BRs) was influenced by changes in nonpulsatile flow through the aortic lumen and 2) to examine the BR and aortic arch responses to changes in temperature. 2. An in vitro aortic arch-aortic nerve preparation was used to record suprathreshold steady-state discharge in a total of 29 single-unit BRs from 12 New Zealand white rabbits. Changes in BR frequency were measured relative to control and were recorded simultaneously with aortic arch pressure, flow, temperature, diameter, and calculated wall shear stress (Sw). 3. With pressure held constant, stair-step increases in flow (3–18 ml/min) constricted the arch and evoked two types of BR responses: activation in most units (15 of 17 BRs tested) and inhibition in 2 units. The activation response appeared closely related to the changes in flow and Sw, but also appeared related to uncontrolled changes in perfusate temperature. 4. When the effects of temperature were examined more closely with pressure and flow held constant, controlled step increases in temperature (between 32 and 42 degrees C) constricted the arch and again evoked two BR responses: activation in 11 of 14 BRs tested and inhibition in 3 units. The Q10 for the activation response was 1.55 +/- 0.08 (mean +/- SE), which was not significantly different from the Q10 for activation when temperature varied with flow (1.65 +/- 0.1, P < 0.05). Thus the effect of temperature on most BRs was directionally and quantitatively similar in the presence and absence of changes in flow. 5. Last, when flow was examined over a wide range (15–515 ml/min) with temperature and pressure held constant, stair-step increases in flow failed to produce any change in BR frequency in each of 15 fibers tested (10 arches). The lack of response was not due to a functionally damaged preparation because the usual BR and aortic arch responses to pressure and to drug-evoked vasoconstriction (norepinephrine) and endothelial-mediated vasodilation (acetylcholine) were intact. 6. These results demonstrate that aortic BRs in rabbits are not sensitive to flow and thus are not likely influenced by fluctuations in cardiac output apart from associated changes in pressure. The aortic BRs are affected directly by variations in temperature and in some cases indirectly by temperature-related vasoconstriction. The effects of temperature may have important implications for neural control of the circulation when core temperature varies because of physiological and environmental stress.

Identification of carotid vascular receptors that control adrenal catecholamine secretion in dogs

1992 ◽  
Vol 262 (5) ◽  
pp. R872-R878
Author(s):  
W. C. Engeland ◽  
C. D. Zippe ◽  
D. S. Gann
Keyword(s):  
Carotid Sinus ◽  
Carotid Occlusion ◽  
Catecholamine Secretion ◽  
Adrenal Vein ◽  
Carotid Baroreceptors ◽  
Cervical Vagotomy ◽  
Anesthetized Dogs ◽  
Reflex Control ◽  
Adrenal Secretion

The role of carotid sinus and thyrocarotid mechanoreceptors in the reflex control of adrenal medullary function was assessed in anesthetized dogs with adrenal vein catheters. Dogs underwent carotid sinus, thyrocarotid junction, combined carotid sinus and thyrocarotid junction, or sham denervation. On the day after surgery, catecholamine secretion was measured after carotid occlusion proximal to the thyrocarotid junction, cervical vagotomy, and repeat carotid occlusion, each separated by 90 min. After combined carotid denervation, baseline norepinephrine secretion was increased, resulting in a decreased epinephrine-to-norepinephrine ratio. Carotid occlusion before vagotomy did not change the secretion of catecholamines or the epinephrine-to-norepinephrine ratio. After sham carotid denervation, acute vagotomy did not affect catecholamine secretion. However, after denervation of the carotid sinus or thyrocarotid junction, vagotomy resulted in small increases in catecholamine secretion without changing the epinephrine-to-norepinephrine ratio; the magnitude of the response was augmented after combined denervation. At 90 min after vagotomy in dogs with intact carotid baroreceptors, carotid occlusion increased adrenal secretion of catecholamines and decreased the epinephrine-to-norepinephrine ratio. After denervation of carotid sinus or thyrocarotid junction receptors, carotid occlusion increased secretion of catecholamines without changing the epinephrine-to-norepinephrine ratio; the response was abolished by combined denervation. These results show that both carotid sinus and thyrocarotid receptors contribute to the adrenomedullary response to carotid occlusion and to acute vagotomy. Also, reduction in the activity of carotid sinus and thyrocarotid junction receptors chronically (by denervation) or acutely (by carotid occlusion) results in preferential secretion of norepinephrine over epinephrine.

Gadolinium and mechanotransduction of rat aortic baroreceptors

1992 ◽  
Vol 262 (5) ◽  
pp. H1415-H1421 ◽  
Author(s):  
M. C. Andresen ◽  
M. Yang
Keyword(s):  
Ion Channels ◽  
Direct Effects ◽  
Cellular Mechanisms ◽  
Pressure Discharge ◽  
Ethanesulfonic Acid ◽  
Discharge Pressure ◽  
Aortic Baroreceptors ◽  
Stretch Activated Channels ◽  
Stretch Activated Ion Channels

The cellular mechanisms enabling baroreceptors to transduce wall distortion into axonal discharge are unknown but might involve stretch-activated ion channels. Gadolinium (Gd3+, 10 microM) blocks stretch-activated channels in several preparations. Here we tested Gd3+ effects on discharge responses of 15 single-fiber baroreceptors in vitro. We simultaneously measured discharge, pressure, and aortic diameter at Gd3+ concentrations from 0.001 to 400 microM. High levels of Gd3+ added to a bicarbonate-buffered perfusate (Krebs) slightly shifted the pressure-discharge relation (less than 4 mmHg, n = 3, P = 0.01) without affecting slope or discharge frequency at threshold. Gd3+ in Krebs variably altered the pressure-diameter relation. Because 500 microM Gd3+ produced visible precipitate in Krebs, we tested Gd3+ in a simpler perfusate using N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES). Gd3+ in HEPES (n = 10) induced minor, but statistically significant, average increases in threshold (less than +5-7%) and no changes in gain. However, prolonged HEPES exposure alone (n = 2) produced similar shifts. Electron microscopy verified that Gd3+ diffused from the lumen to reach extracellular locations near baroreceptor endings. We conclude that 1) HEPES perfusate alone reversibly depresses baroreceptor discharge and 2) Gd3+ has no direct effects on baroreceptors. Thus it appears that aortic baroreceptor mechanotransduction must utilize a different class of stretch-activated ion channels.

Direct action of norepinephrine on aortic baroreceptors of rat adventitia

1984 ◽  
Vol 247 (5) ◽  
pp. H811-H816 ◽  
Author(s):  
D. L. Kunze ◽  
J. M. Krauhs ◽  
C. J. Orlea
Keyword(s):  
Smooth Muscle ◽  
Aortic Arch ◽  
Direct Action ◽  
Muscle Tension ◽  
Cyclic Stretch ◽  
Direct Effects ◽  
Adrenergic Modulation ◽  
Aortic Baroreceptors

The adventitia of the rat aortic arch, with the depressor nerve intact, was separated from the underlying media to obtain a preparation in which the direct effects of norepinephrine on baroreceptor discharge could be examined free of smooth muscle effects. Cyclic stretch was applied to the adventitia to evoke discharge in single aortic baroreceptor fibers. Norepinephrine and phenylephrine in concentrations of 10(-7) to 10(-5) M increased baroreceptor discharge. No effect on discharge was seen with isoproterenol. Phentolamine but not propranolol blocked the increase in discharge produced by norepinephrine. An alpha-adrenergic modulation of baroreceptor discharge that is not dependent on smooth muscle tension has been demonstrated.

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