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V S Bishop

Publications and source records attributed to V S Bishop.

At least 19 recordsLinked to original sources
PubMed1995

Effects of arginine vasopressin and angiotensin II on area postrema neurons in rabbit brain slice preparation.

Previous in vivo studies have indicated that both arginine vasopressin (AVP) and angiotensin II (ANG II) can modulate the baroreflex by acting on the area postrema (AP). In the present study, effects of AVP and ANG II on AP neuronal activity were investigated by recording extracellular activity in a rabbit brainstem slice preparation. AVP (1 nM-1 microM) inhibited 14.5% and excited 53.2% of the neurons while ANG II (1 nM-5 microM) inhibited 32.3% and excited 29% of the neurons. Application of AVP and ANG II to the same AP neurons at the same concentration indicated that more AP neurons responded to AVP than to ANG II. ANG II induced more inhibitory responses than AVP. The results suggest that AVP and ANG II may produce different effects on the baroreflex by acting on different pools of AP neurons and by exerting different effects on the same AP neuron.

Action Potentials↗
PubMed1995

Pregnancy attenuates activity of the baroreceptor reflex.

1. Pregnancy-induced changes in acute blood pressure regulation are reviewed. 2. Pregnant animals are less able to maintain arterial pressure during haemorrhage than non-pregnant animals. 3. Baroreceptor reflex-mediated increases in heart rate, renal sympathetic activity, vasopressin, ACTH and cortisol are reduced during pregnancy. Therefore, one explanation for the subnormal ability of pregnant animals to regulate arterial pressure during haemorrhage is that the baroreceptor reflex is not as effective. 4. Chronic increases in oestrogen levels in non-pregnant rabbits do not reduce the gain of baroreflex control of renal sympathetic activity. This and other findings suggest that oestrogen alone does not mediate the blunted baroreflex activity observed during pregnancy.

Animals↗
PubMed1995

Permissive role for nitric oxide in active thermoregulatory vasodilation in rabbit ear.

The present study was designed to test the hypothesis that during whole body heating (WBH), nitric oxide (NO) synthesized in the endothelium acts synergistically with an unknown neurotransmitter to elicit active vasodilation. Rabbits were instrumented for the measurement of mean arterial pressure, heart rate, and ear blood flow (EBF) (Doppler ultrasound). During WBH, either N omega-nitro-L-arginine methyl ester (L-NAME, 10-40 mg over 10-15 min, n = 6 rabbits; group 1), a NO synthase inhibitor, or saponin (30-40 mg over 10-20 min, n = 6 rabbits; group 2), a detergent that denudes the endothelium, was given via a lingual artery catheter until thermoregulatory vasodilation was reversed. When EBF stabilized at the new reduced level, the NO donor, sodium nitroprusside (SNP), was infused (0.2-1.0 mg/ml, 0.01-0.05 ml/min, 2-5 min) via the lingual artery catheter. During WBH, EBF increased from 0.39 +/- 0.08 to 6.47 +/- 0.63 kHz in group 1, and from 0.69 +/- 0.18 to 5.72 +/- 0.49 kHz in group 2. Infusion of L-NAME decreased EBF in group 1 to 1.97 +/- 0.40 kHz. Infusion of saponin decreased EBF in group 2 to 1.23 +/- 0.40 kHz. Subsequent SNP infusion during hyperthermia returned EBF to 6.88 +/- 0.72 kHz in group 1 and 5.53 +/- 1.27 kHz in group 2 but had no effect when administered during normothermia. These results suggest that NO acts in conjunction with another substance, presumably the neurotransmitter released on WBH, to elicit thermoregulatory vasodilation.

Animals↗
PubMed1995

Angiotensin II modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism in rabbits.

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on baroreflex function curves before and after intravertebral administration of the alpha 1-adrenoreceptor antagonist prazosin. Rabbits were chronically instrumented with subclavian and vertebral arterial catheters, venous catheters, and aortic and vena caval occludes. Baroreflex curves were obtained by relating heart rate (HR) to mean arterial pressure during increases and decreases in arterial pressure. Intravertebral infusions of ANG II (5, 10, and 20 ng.kg-1.min-1) produced a dose-dependent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretreatment with prazosin (10 micrograms/kg) via the vertebral artery markedly reduced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II resets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha 1 mechanism. When the effects of vertebral ANG II on the baroreflex control of renal sympathetic nerve activity (RSNA) were examined, intravertebral administration of ANG II, while reducing the gain and the maximum RSNA, did not reset the RSNA baroreflex curve. These data suggest that ANG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha 1-adrenergic mechanism.

Adrenergic alpha-Antagonists↗
PubMed1992

Onset of exercise shifts operating point of arterial baroreflex to higher pressures.

This study was designed to test the hypothesis that the increase in sympathetic nerve activity (SNA) and mean arterial pressure (MAP) at the onset of exercise is dependent on a rapid upward shift of the operating point of the arterial baroreflex. To test this hypothesis, we recorded renal sympathetic nerve activity (RSNA) in 16 New Zealand White rabbits during treadmill running (12.6 m/min, 20% grade) under control conditions and during concomitant intravenous infusions of nitroglycerin (NTG) to attenuate the exercise pressor response. In the control condition, MAP increased 18 +/- 2 mmHg. This was associated with an increase in heart rate (HR) (104 +/- 4 beats/min) and RSNA (414 +/- 20%). The increases in RSNA (848 +/- 32%) and HR (155 +/- 5 beats/min) at the onset of exercise were significantly augmented when the rate of development of the exercise pressor response (0.3 +/- 0.03 to 0.12 +/- 0.01 mmHg/s) and the magnitudes of the pressor response (91 +/- 2 to 79 +/- 1 mmHg) were attenuated by infusions of NTG. These data suggest that at the onset of exercise the operating point of the arterial baroreflex is reset toward higher pressures. The MAP, RSNA, and HR responses to exercise were also determined in eight sinoaortic-denervated (SAD) rabbits. In the absence of a functional baroreflex, MAP (-46 +/- 2 mmHg), RSNA (-19 +/- 1%), and HR (-62 +/- 3 beats/min) decreased at the onset of exercise and recovered 1 min to -42 +/- 2, +13 +/- 1, and +9 +/- 1% of control, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Effect of fasting and refeeding on mesenteric autoregulation in conscious rabbits.

To determine whether feeding improves the efficacy of mesenteric autoregulation in conscious animals, rabbits were instrumented with pulsed-Doppler flow probes on the superior mesenteric artery and distal abdominal aorta to record mesenteric and hindquarters blood flow velocity. Hydraulic occluders were placed on the abdominal aorta (just below the celiac artery) and the thoracic vena cava to vary mesenteric and hindquarters arterial pressure (MAP), which was monitored via a catheter positioned in the distal abdominal aorta. Heart rate (HR) and lumbar sympathetic nerve activity (LSNA) were monitored as indexes of sympathetic nervous system activity. Pressure-velocity curves were obtained by aortic and caval occlusions on two consecutive days; first after a 24-h fast and after approximately 24 h of ad libitum refeeding. In the fed state, mesenteric velocity was significantly increased and MAP was decreased slightly; the slight decrease in MAP was counteracted by significant increases in HR and LSNA, whereas hindquarters perfusion was unchanged. The mesenteric and hindquarters pressure-velocity curves were all highly linear (r greater than or equal to 0.9) and showed no evidence of autoregulation in the fasted or fed state when pressure was changed by either the aortic or the caval occlusions. We conclude that autoregulation plays a minor role in the short-term regulation of mesenteric blood flow in the conscious rabbit.

Animals↗
PubMed1992

Neurogenic vasodilator control of rabbit ear blood flow.

Ear blood flow subserves thermoregulation in the rabbit. The purpose of this study was to determine if the increase in rabbit ear blood flow, in response to increases in internal temperature (Ti) of approximately 2 degrees C (38.0-40.0 degrees C), is due to an active vasodilation or a withdrawal of adrenergic vasoconstrictor activity. New Zealand White rabbits were chronically instrumented with a pulse Doppler flow probe on the central ear artery of the left and right ear for the measurement of ear blood flow velocity (EBF, kHz). Catheters were also positioned in one occipital artery for selective administration of an alpha 1-adrenergic antagonist to one ear, while the contralateral ear served as a control. During hyperthermia (H) (increase in rectal temperature) alpha 1-adrenergic blockade had no effect on the maximum EBF (5.95 +/- 0.87 before vs. 6.11 +/- 1.04 kHz after). However, alpha 1-adrenergic blockade increased resting EBF during normothermia from 0.18 +/- 0.04 to 1.23 +/- 0.27 kHz (P less than 0.05), suggesting that a decrease in alpha 1-adrenergic tone may account for approximately 20% of the increase in EBF during heating. The second protocol was designed to determine if blockade of the auricular nerve would alter EBF response to H. During maximum EBF during H, saline or procainamide was injected in the tissue surrounding the auricular nerve. Injection of procainamide decreased EBF from 5.99 +/- 0.87 to 0.48 +/- 0.19 kHz, while injection of saline had no effect on EBF of the contralateral ear (4.33 +/- 1.16 before vs. 3.97 +/- 1.04 kHz after).(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1992

Vasopressin-induced suppression of renal sympathetic outflow depends on the number of baroafferent inputs in rabbits.

We tested the hypothesis that the inhibitory action of arginine vasopressin (AVP) on renal sympathetic nerve activity (RSNA) is related to the number of baroreceptor stations. The role of baroreceptor afferents was determined by comparing the effects of AVP on the baroreflex function curves [mean arterial pressure (MAP) vs. %RSNA] obtained in intact conscious rabbits with those obtained in rabbits with one carotid sinus and one aortic nerve intact (1CSN + 1AoN) and in rabbits with only a single carotid sinus nerve intact (1CSN). Baroreflex curves were obtained by relating %RSNA to MAP during ramp increases and decreases in MAP. MAP was increased with phenylephrine and decreased with caval occlusion. In the intact state (n = 7), AVP infusions (0.4, 1.5, and 3.0 mU.kg-1 x min-1) produced dose-dependent reduction in the maximum %RSNA (97 +/- 1 to 85 +/- 6, 68 +/- 6, and 57 +/- 5%, respectively) at minimum MAP and the gain of the baroreflex curve (5.7 +/- 0.2 to 3.9 +/- 0.2, 3.2 +/- 0.3, and 2.2 +/- 0.2 mmHg, respectively) and shifted the midrange of the curves (72 +/- 3 to 68 +/- 4, 68 +/- 2, and 63 +/- 3 mmHg, respectively). However, in the 1CSN + 1AoN state (n = 6), the medium dose of AVP (1.5 mU.kg-1 x min-1) did not significantly alter the maximum %RSNA, the gain of the curve, or the midrange of the curve. The highest dose of AVP (3.0 mU.kg-1 x min-1) still reduced the maximum %RSNA (98 +/- 3 to 75 +/- 3) and the gain of the curve (4.1 +/- 0.4 to 2.7 +/- 0.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1991

Role of baroreceptor afferents on area postrema-induced inhibition of sympathetic activity.

Activation of the area postrema by either electrical stimulation or chemical application of L-glutamate has been shown to result in an enhancement of cardiovascular baroreflexes similar to that seen with systemic infusions of arginine vasopressin (AVP). In addition, it has been found that the effects of AVP on baroreflex inhibition of renal sympathetic nerve activity (RSNA) are similar to those observed with phenylephrine following lesions of the area postrema or after partial denervation of baroreceptor afferents. The present study was undertaken to determine the role of baroreceptor afferent input on area postrema stimulation-induced decreases in sympathetic activity. In anesthetized rabbits, the responses of arterial pressure, heart rate, and RSNA to area postrema electrical stimulation were obtained before and after progressive sinoaortic denervation and vagotomy. Stimulation of the area postrema in carotid sinus-denervated animals consistently decreased RSNA in a frequency-dependent manner. However, following bilateral removal of both the aortic nerves and the vagi, electrical stimulation of the area postrema had no effect on RSNA. These results suggest that the ability of area postrema stimulation to inhibit RSNA is dependent on the presence of baroreceptor afferent input.

Afferent Pathways↗
PubMed1991

Effects of area postrema stimulation on neurons of the nucleus of the solitary tract.

Previous studies have suggested that neurons of the area postrema may modulate cardiovascular function through an interaction at the level of the nucleus of the solitary tract (NTS). Using an in vitro brain slice preparation of the rabbit medulla, the present study investigated the electrophysiological and pharmacological effects of area postrema stimulation on NTS neuronal activity. In the majority of neurons tested (85.7%), electrical stimulation of the area postrema consistently produced either single or multiple action potentials in NTS neurons. Latency values for neurons showing single spike responses to area postrema stimulation ranged from 3.0 to 17.0 ms with an average latency of 9.3 +/- 4.3 ms. The average threshold for area postrema activation of these nonspontaneously active NTS neurons was 99.8 +/- 12 microA with a stimulus threshold range between 15 and 200 microA (n = 53). Perfusion of the slice with phentolamine (1.0 microM) or yohimbine (200 nM) blocked the area postrema-evoked action potentials, whereas perfusion of the slice with prazosin (200 nM) had no effect. These findings suggest that area postrema neurons do modulate NTS neuronal activity and that this modulation results in an increase in NTS neuronal activation.

Afferent Pathways↗
PubMed1991

Interactions of area postrema and solitary tract in the nucleus tractus solitarius.

The nucleus tractus solitarius (NTS) receives information from both area postrema (AP) and peripheral afferents. It is, therefore, one likely site of interaction between AP and peripheral afferent fibers. The present study's purpose was to determine the influence of AP stimulation on solitary tract-induced modulation of NTS neuronal activity. With the use of an in vitro rabbit brain slice preparation, extracellular recordings were made from 58 NTS neurons in which action potentials were evoked by both solitary tract and AP stimulation. In the majority of the cells tested, simultaneous stimulation of solitary tract and AP, at voltage levels that evoked no action potentials when stimulated separately, resulted in production of either single or multiple action potentials. In 27 units, stimulation levels to the solitary tract and to the AP were adjusted such that their respective separate stimulations produced an NTS action potential less than 30% of the time. When the two inputs were stimulated together, simultaneous stimulations produced an NTS action potential 100% of the time, suggesting a facilitatory interaction between the AP and the solitary tract on NTS neuronal activity. In nine cells, perfusion of the slice with clonidine induced a facilitation of solitary tract-evoked NTS response to a level similar to that seen during simultaneous stimulation of the solitary tract with the AP. Application of the alpha 2-adrenergic receptor antagonist yohimbine blocked the ability of both clonidine and AP to facilitate the solitary tract-evoked response. These results support a possible interaction between AP and peripheral afferents and suggest that AP stimulation facilitates effects of solitary tract activation at the level of the NTS.

Action Potentials↗
PubMed1991

Neural and humoral mechanisms of angiotensin-dependent hypertension.

We examined whether neural or humoral mechanisms mediate the acute versus chronic phases of angiotensin II (ANG II)-dependent hypertension in rabbits. ANG II was administered intravenously at 50 ng.kg-1.min-1 for 10 days. This dose of ANG II elevated mean arterial pressure (MAP) from 76 +/- 2 to 98 +/- 2 mmHg on day 1 and sustained the hypertension throughout the infusion period. Heart rate (226 +/- 7 beats/min) was not altered. The depressor response to ganglionic blockade (-38 +/- 2 mmHg) was significantly blunted on day 1 (-22 +/- 3 mmHg) and was significantly enhanced on days 5 (-52 +/- 4 mmHg) and 7 (-52 +/- 6 mmHg). In contrast, plasma norepinephrine (PNE) and renal sympathetic nerve activity (RSNA) levels were acutely reduced to approximately one-third of control (day 1 of ANG II) and chronically rose to an intermediate level (2-9 days of ANG II). However, the pressor effect of resetting PNE and RSNA may be magnified by an augmented pressor responsiveness to alpha-agonists after chronic ANG II. In animals with the area postrema removed, PNE, RSNA, and heart rate were acutely reduced and remained chronically depressed. In addition, area postrema lesion blocked the chronic, but not the acute hypertensive response, to infusing ANG II. Thus the direct vasoconstrictor actions of ANG II appear to acutely predominate, whereas neurogenic vasomotor tone appears to chronically predominate. This shift appears to be mediated by changes in vascular sensitivity, as well as the area postrema allowing resetting of the baroreflex.

Angiotensin II↗
PubMed1990

Exercise training enhances cardiac afferent inhibition of baroreflex function.

The influence of cardiac afferents on the arterial baroreflex regulation of renal sympathetic nerve activity (RSNA) was examined before and after an endurance training program. The 8-wk endurance exercise training program resulted in an exercise-induced bradycardia (decreased heart rates at rest and during a graded exercise test). At rest (210 +/- 6 vs. 242 +/- 10 beats/min) and during treadmill running at 15.0 m/min, 20% grade (287 +/- 5 vs. 390 +/- 5 beats/min) posttraining heart rates were lower than pretraining. In addition, when compared with a group of untrained rabbits, trained rabbits had a significantly higher heart weight-to-body weight ratio (1.9 +/- 0.02 vs. 2.8 +/- 0.017 g/kg). Rabbits were instrumented with a Doppler flow probe around the ascending aorta, Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves and catheters in the central ear artery and vein. Before training, cardiac afferent blockade (intrapericardial procainamide, 2%) did not significantly alter resting mean arterial pressure, cardiac index, systemic vascular resistance index or RSNA. After training, intrapericardial procainamide mean arterial pressure increased (P less than 0.05) resting (75 +/- 4 to 86 +/- 3 mmHg) and RSNA (100% to 175 +/- 15%). More importantly, cardiac afferent blockade did not alter the range (106 +/- 4 vs. 103 +/- 4%) or gain (4.1 +/- 0.3 vs. 3.4 +/- 0.3%/mmHg) of the baroreflex function curve in the untrained rabbit. However, after training, cardiac afferent blockade increased (P less than 0.05) the range (55 +/- 3 to 103 +/- 4%) and gain (1.5 +/- 0.07 to 3.9 +/- 0.2%/mmHg) of baroreflex regulation of RSNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1990

Regional vascular resistance during exercise: role of cardiac afferents and exercise training.

This study was designed to determine whether cardiac vagal afferents exert an inhibitory influence on increases in regional vascular resistance during exercise and to determine whether endurance exercise training enhances the inhibitory influence of cardiac vagal afferents. We measured changes in regional vascular resistance in 12 rabbits at rest and during running at 12.6 m/min, 20% grade, before and after reversible denervation of cardiac afferents (intrapericardial procainamide HCl, 2%). In addition, these procedures were repeated in five of these rabbits following an 8-wk endurance exercise training program. Because intrapericardial injections of procainamide anesthetize both the efferent as well as the afferent innervation to the heart, it was necessary to determine the effects of blocking the efferent innervation on the regulation of regional vascular resistance during exercise. Rabbits were instrumented with Doppler ultrasonic flow probes around the renal (R), mesenteric (M), ascending, and terminal aortic (TA) arteries. Catheters were positioned in the central ear artery and vein and pericardial sac. Mean arterial pressure, heart rate, cardiac output, R, M, TA, and systemic (S) resistances were determined. Exercise changed R (+37 +/- 4%), M (+88 +/- 9%), TA (-62 +/- 6%), and S (-34 +/- 3) resistances. Subsequent cardiac efferent blockade alone had no significant effect on regional vascular resistance during exercise. Combined efferent and afferent blockade resulted in significant increases in R (+62 +/- 6%) and M resistance (+134 +/- 13%) but did not alter TA (-51 +/- 4%) or S (-27 +/- 2%) resistance during exercise. Exercise training significantly enhanced the inhibitory influence of cardiac afferents on R and M regional vascular resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1990

Neurons in area postrema mediate vasopressin-induced enhancement of the baroreflex.

Intravenous infusion of arginine vasopressin (AVP) has been shown to enhance baroreflex sensitivity, and this enhancement is dependent on the integrity of the area postrema. However, previous studies did not differentiate a role for cell bodies in the area postrema vs. the dense network of fibers located in and around the lateral and ventral margins of this circumventricular organ. In the present study, baroreflex function was assessed in conscious rabbits by examining heart rate after ramp infusions of phenylephrine (PE) and AVP. The subsequent day, the excitotoxin kainic acid was injected (30 nl initially, with five 15-nl supplemental injections of a 1 ng/nl solution over 1 h) into the area postrema, thus selectively destroying cell bodies. After an 8-day recovery period, baroreflex function was again assessed. The bradycardic response to graded infusion of PE (slope = -2.29 +/- 0.30) was not significantly different after selective lesions of area postrema neurons (slope = -1.88 +/- 0.49). In contrast, the previously enhanced bradycardic response to infusion of AVP (slope = -5.76 +/- 1.02) was significantly attenuated (slope = -2.31 +/- 0.21) to levels similar to that seen with infusion of PE. Thus selective chemical lesions of area postrema neurons block vasopressin-induced enhancement of the baroreflex.

Animals↗
PubMed1990

Cardiovascular and neuroendocrine responses to baroreceptor denervation in baboons.

The purpose of this study was to describe the hormonal and blood pressure responses to partial (carotid sinus) and complete (carotid sinus + aortic arch) baroreceptor denervation in baboons. Experiments were performed in eight adult male baboons maintained on a tether system for the continuous measurement of mean arterial blood pressure (MAP) and heart rate (HR). Bilateral carotid sinus denervation (CSD) immediately increased MAP from 83 +/- 2.2 to 124 +/- 7.3 mmHg. MAP gradually decreased over the next 14 days to intact levels. There were also transient decreases in HR variability and increases in blood pressure variability after CSD. Subsequent denervation of the aortic arch to produce sinoaortic denervation (SAD) resulted in another abrupt large increase in MAP followed by a small but significant increase in MAP of 11 mmHg that was maintained for up to 4 wk after SAD. The short-term variability of HR and blood pressure was chronically decreased and increased, respectively, after SAD. Plasma renin activity, vasopressin, and epinephrine were not changed from intact levels either after CSD or SAD. Plasma norepinephrine was only transiently increased by CSD and chronically elevated by 72% over intact levels after SAD. Thus CSD in the baboon does not produce a sustained increase in MAP. SAD chronically increases MAP and is associated with evidence for an increased sympathetic tone. There is no indication that either increased renin secretion or vasopressin secretion contributes to the chronic cardiovascular effects of SAD in baboons.

Animals↗
PubMed1990

Reflex effect of vasopressin after blockade of V1 receptors in the area postrema.

This study investigated the effect of micropressure injection of the V1 arginine vasopressin (AVP) receptor antagonist into the area postrema on the ability of circulating AVP to augment baroreflex inhibition of renal sympathetic nerve activity (RSNA) in urethane-anesthetized rabbits. In addition, the effects of micropressure injections of AVP into the area postrema on RSNA, arterial pressure, heart rate, and baroreflex control of RSNA were evaluated. Injection of 100 ng (in a 10-nl volume) of AVP antagonist into the area postrema abolished the ability of AVP to enhance baroreflex inhibition of RSNA compared with phenylephrine (-8.84 +/- 0.89 before antagonist versus -4.83 +/- 0.44 %RSNA/mm Hg after antagonist). Normal baroreflex inhibition to phenylephrine (-3.95 +/- 0.26 versus -4.10 +/- 0.33 %RSNA/mm Hg) was unaltered. This dose of AVP antagonist given intravenously or into the adjacent medial nucleus tractus solitarius was without effect. Micropressure injection of AVP directly into the area postrema produced a dose-dependent decrease in RSNA without significant effects on arterial pressure or heart rate. Local injection of 4 +/- 0.6 ng (in a 4-nl volume) of AVP produced an average 27 +/- 3% decrease in resting RSNA. Continuous injection of AVP into the area postrema using short-duration, low-frequency pressure pulses significantly augmented the baroreflex inhibition of RSNA during phenylephrine infusion (during AVP injection, -7.12 +/- 1.60%RSNA/mm Hg; control, -3.38 +/- 0.55 %RSNA/mm Hg). These data support the hypothesis that circulating AVP acts at the area postrema to augment baroreflex inhibition of RSNA by a V1 receptor mechanism.

Animals↗