Arterial Baroreceptors: Excitation and Modulation

2020 ◽  
pp. 139-164 ◽  
Author(s):  
Diana L. Kunze ◽  
Michael C. Andresen
Keyword(s):  
Arterial Baroreceptors

Effects of water immersion on arginine vasopressin release in humans

1988 ◽  
Vol 64 (1) ◽  
pp. 1-10 ◽  
Author(s):  
P. Norsk ◽  
M. Epstein
Keyword(s):  
Water Intake ◽  
Arginine Vasopressin ◽  
Critical Review ◽  
Water Immersion ◽  
Base Line ◽  
Vasopressin Release ◽  
Arterial Baroreceptors ◽  
Lower Base

Since suppression of arginine vasopressin (AVP) appears to be a determinant of the diuresis of water immersion (WI) in humans, a further understanding of its responsiveness has important implications for normal physiology, pathophysiology, and space physiology. In recent years, discrepant measurements of AVP in plasma during WI have led to conflicting conclusions. In studies in which the subjects ingested water before or during WI, plasma AVP was reported to be unchanged or even increased. In contrast, plasma AVP was suppressed in studies in which the subjects remained hydropenic. A critical review discloses that water intake before and/or during the experiments introduces several new stimuli for AVP release. Furthermore the lower base-line levels of AVP in hydrated subjects complicate detection of small changes in plasma AVP. Although the mechanisms of AVP suppression during WI are incompletely defined, it appears that not only cardiopulmonary mechanoreceptors but also arterial baroreceptors mediate the response. Additional studies are proposed to delineate further the mechanisms governing AVP release during WI.

Mechanisms of Resetting of Arterial Baroreceptors: An Overview

1988 ◽  
Vol 295 (4) ◽  
pp. 327-334 ◽  
Author(s):  
Mark W. Chapleau ◽  
George Hajduczok ◽  
Francois M. Abboud
Keyword(s):  
Arterial Baroreceptors

scholarly journals Evidence for unloading arterial baroreceptors during low levels of lower body negative pressure in humans

2009 ◽  
Vol 296 (2) ◽  
pp. H480-H488 ◽  
Author(s):  
Qi Fu ◽  
Shigeki Shibata ◽  
Jeffrey L. Hastings ◽  
Anand Prasad ◽  
M. Dean Palmer ◽  
...  
Keyword(s):  
Steady State ◽  
Stroke Volume ◽  
Negative Pressure ◽  
Lower Body Negative Pressure ◽  
Right Atrial ◽  
Lower Body ◽  
Arterial Baroreflex ◽  
Arterial Baroreceptors ◽  
Low Levels ◽  
Cardiopulmonary Baroreceptors

Low levels (i.e., ≤20 mmHg) of lower body negative pressure (LBNP) have been utilized to unload “selectively” cardiopulmonary baroreceptors in humans, since steady-state mean arterial pressure and heart rate (HR) have been found unchanged at such levels. However, transient reductions in blood pressure (BP), followed by reflex compensation, may occur without detection, which could unload arterial baroreceptors. The purposes of this study were to test the hypothesis that the arterial baroreflex is engaged even during low levels of LBNP and to determine the time course of changes in hemodynamics. Fourteen healthy individuals (age range 20–54 yr) were studied. BP (Portapres and Suntech), HR (ECG), pulmonary capillary wedge pressure (PCWP) or pulmonary artery diastolic pressure (PDP) and right atrial pressure (RAP) (Swan-Ganz catheter) and hemodynamics (Modelflow) were recorded continuously at baseline and −15- and −30-mmHg LBNP for 6 min each. Application of −15-mmHg LBNP resulted in rapid and sustained falls in RAP and PCWP or PDP, progressive decreases in cardiac output and stroke volume, followed subsequently by transient reductions in both systolic and diastolic BP, which were then restored through the arterial baroreflex feedback mechanism after ∼15 heartbeats. Additional studies were performed in five subjects using even lower levels of LBNP, and this transient reduction in BP was observed in three at −5- and in all at −10-mmHg LBNP. The delay for left ventricular stroke volume to fall at −15-mmHg LBNP was about 10 cardiac cycles. An increase in systemic vascular resistance was detectable after 20 heartbeats during −15-mmHg LBNP. Steady-state BP and HR remained unchanged during mild LBNP. However, BP decreased, while HR increased, at −30-mmHg LBNP. These results suggest that arterial baroreceptors are consistently unloaded during low levels (i.e., −10 and −15 mmHg) of LBNP in humans. Thus “selective” unloading of cardiopulmonary baroreceptors cannot be presumed to occur during these levels of mild LBNP.

scholarly journals Role of arterial baroreceptors on commissural NTS (cNTS) neurons involved in hemodynamic (Hd) control

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Monica Akemi Sato ◽  
Shaun F Morrison ◽  
Oswaldo U Lopes ◽  
Eduardo Colombari
Keyword(s):  
Arterial Baroreceptors

Cardiovascular afferent inputs to ventral tegmental area

1997 ◽  
Vol 272 (6) ◽  
pp. R1998-R2003 ◽  
Author(s):  
G. J. Kirouac ◽  
J. Ciriello
Keyword(s):  
Ventral Tegmental Area ◽  
Discharge Rate ◽  
Onset Latency ◽  
Selective Activation ◽  
Unit Recording ◽  
Arterial Baroreceptors ◽  
Reflex Activation ◽  
Afferent Inputs ◽  
Ventral Tegmental ◽  
Stimulation Of

Extracellular single-unit recording experiments were done in alpha-chloralose-anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of selective activation of arterial baroreceptors and stimulation of cardiovascular depressor sites in the nucleus of the solitary tract (NTS) on the discharge rate of neurons in the ventral tegmental area (VTA). Electrical stimulation of the aortic depressor nerve (ADN), which is known to carry aortic baroreceptor afferent fibers only, excited 12 of 21 (mean onset latency 42.4 +/- 8.8 ms) and inhibited 2 of 21 (mean onset latency 42.5 +/- 6.5 ms) single units in the VTA. The discharge rate of VTA units was also altered during the reflex activation of arterial baroreceptors by the acute rise in arterial pressure (AP) to systemic injections of phenylephrine (10 micrograms/kg i.v.): 12 of 44 units were excited and 15 of 44 were inhibited. Units that responded to either ADN stimulation or the reflex activation of the baroreflex also responded to stimulation of depressor sites in the NTS. An additional 12 units that were found in barodenervated controls to be responsive to NTS stimulation were nonresponsive to selective activation of arterial baroreceptors. These data indicate that cardiovascular afferent inputs modulate the activity of neurons in the VTA and suggest that changes in systemic AP may exert an effect on the activity of neurons involved in mesolimbic and mesocortical function.

scholarly journals Arterial Baroreceptors Sense Blood Pressure through Decorated Aortic Claws

Cell Reports ◽  
2019 ◽  
Vol 29 (8) ◽  
pp. 2192-2201.e3 ◽  
Author(s):  
Soohong Min ◽  
Rui B. Chang ◽  
Sara L. Prescott ◽  
Brennan Beeler ◽  
Narendra R. Joshi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Baroreceptors

Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear

1997 ◽  
Vol 83 (6) ◽  
pp. 2091-2097 ◽  
Author(s):  
Kathy L. Ryan ◽  
W. Fred Taylor ◽  
Vernon S. Bishop
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Whole Body ◽  
Arterial Baroreflex ◽  
Animal Group ◽  
Arterial Baroreceptors ◽  
Mechanical Unloading ◽  
Rabbit Ear ◽  
Cardiac Afferents ◽  
Plateau Level

Ryan, Kathy L., W. Fred Taylor, and Vernon S. Bishop.Arterial baroreflex modulation of heat-induced vasodilation in the rabbit ear. J. Appl. Physiol. 83(6): 2091–2097, 1997.—The purpose of this study was to determine whether nonthermal baroreflexes arising from cardiopulmonary and/or arterial baroreceptors modulate rabbit ear blood flow (EBF) during hyperthermia. Intact and sinoaortic-denervated (SAD) rabbits were chronically instrumented with a Doppler ultrasonic flow probe for measurement of EBF velocity (kHz). During whole body heating in conscious rabbits, EBF and ear vascular conductance (EVC) increased as core temperature increased until maximal plateau levels of EBF and EVC were reached. The maximal plateau level of EVC attained during heat stress was lower in SAD than in intact rabbits. Subsequent intrapericardial administration of procaine at maximal EBF blocked cardiac afferents but did not alter EVC in either animal group. In a second experiment, ramp decreases in mean arterial pressure were produced by vena caval occlusion at maximal EBF. In intact rabbits, EBF and EVC decreased linearly as mean arterial pressure fell, but EBF and EVC did not decrease during vena caval occlusion in SAD rabbits. Thus neither pharmacological nor mechanical unloading of cardiac baroreceptors results in reflex vasoconstriction in the heat-stressed rabbit ear. However, baroreflexes arising from arterial baroreceptors may modulate EBF in heat-stressed rabbits.

Baroreflex attenuates pressor response to graded muscle ischemia in exercising dogs

1990 ◽  
Vol 258 (2) ◽  
pp. H305-H310 ◽  
Author(s):  
D. D. Sheriff ◽  
D. S. O'Leary ◽  
A. M. Scher ◽  
L. B. Rowell
Keyword(s):  
Perfusion Pressure ◽  
Pressor Response ◽  
Vascular Occlusion ◽  
Arterial Baroreceptors ◽  
Systemic Pressure ◽  
Muscle Ischemia ◽  
Pressor Responses ◽  
Before And After ◽  
Muscle Chemoreflex ◽  
Arterial Baroreceptor

Graded reductions in hindlimb perfusion in dogs exercising at 2 miles/h (0% grade) elicited reflex pressor responses by what is referred to as the “muscle chemoreflex.” To determine the extent to which arterial baroreceptor reflexes oppose the muscle chemoreflex, we elicited pressor responses to muscle ischemia before and after chronic surgical denervation of the arterial baroreceptors. The muscle chemoreflex showed a threshold beyond which systemic pressure rose approximately 3 mmHg for each 1-mmHg decrease in hindlimb perfusion pressure when the arterial baroreceptors were intact. Arterial baroreceptor denervation approximately doubled the pressor responses, i.e., systemic pressure rose by approximately 6 mmHg for each 1-mmHg fall in hindlimb perfusion pressure, without alteration in threshold. We conclude that during mild dynamic exercise, the arterial baroreflexes oppose the pressor response to graded reductions in hindlimb perfusion, reducing it by approximately 50%. When unopposed by the arterial baroreflexes the muscle chemoreflex exhibits a gain (ratio of change in systemic pressure to change in hindlimb perfusion pressure) of approximately -6; thus this reflex can correct by 85% the decrease in muscle perfusion pressure caused by partial vascular occlusion.

Left heart and arterial baroreceptors interact in control of plasma vasopressin, renin, and cortisol in awake dogs

1994 ◽  
Vol 266 (3) ◽  
pp. R879-R888 ◽  
Author(s):  
J. L. Andersen ◽  
L. J. Andersen ◽  
T. N. Thrasher ◽  
L. C. Keil ◽  
D. J. Ramsay
Keyword(s):  
Vena Cava ◽  
Plasma Renin ◽  
Significant Rise ◽  
Atrial Pressure ◽  
Right Atrial ◽  
Arterial Hypotension ◽  
Left Heart ◽  
Arterial Baroreceptors ◽  
Plasma Arginine ◽  
Stimulation Of

Arterial hypotension induced by constriction of the ascending aorta (AA) causes increases in left atrial pressure (LAP) and plasma atrial natriuretic peptide (ANP), but no change in plasma arginine vasopressin (AVP), plasma renin activity (PRA), or cortisol. In the present study, we tested the hypothesis that the rise in left heart pressure during constriction of the AA suppressed the stimulation of AVP, renin, and cortisol secretion in response to arterial hypotension. Dogs were prepared with inflatable cuffs around the AA, the pulmonary artery (PA), and the thoracic inferior vena cava (IVC) and with catheters in the left and right atria and abdominal aorta. In one series of experiments, the AA was constricted to lower mean arterial pressure (MAP) 10 or 20% below control for 15 min. Then, either the PA or the IVC was constricted to bring LAP back to control levels but without altering the degree of arterial hypotension. Constriction of the AA alone led to significant increases in LAP and plasma ANP but no change in plasma AVP, cortisol, or PRA. Reducing LAP to control levels by constriction of either the PA or IVC led to significant and similar increases in plasma AVP, cortisol, and PRA. Plasma ANP fell significantly 10 min after LAP was normalized by constriction of the IVC but not when LAP was normalized by constriction of the PA, because PA constriction caused a significant rise in right atrial pressure that stimulated ANP secretion. The increases in plasma AVP and PRA after normalizing LAP by constriction of the PA were compared with the increases obtained during identical falls in MAP induced by constriction of the IVC alone, a maneuver that lowers LAP below control. The increases in plasma AVP in the two conditions were identical, indicating that the stimulation of left heart baroreceptors alone can account for the suppression of AVP secretion in response to unloading arterial baroreceptors. In contrast, there was a greater rise in PRA during hypotension caused by constriction of the IVC alone compared with the condition in which LAP was normalized but plasma ANP remained elevated. This suggests that increased left heart pressure inhibits renin secretion in response to arterial hypotension by reflex mechanisms and by increased plasma ANP concentration.

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