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Biomedical subjects

E M Hasser

Publications and source records attributed to E M Hasser.

At least 37 records · Page 2Linked to original sources
PubMed1997

Interactions between vasopressin and baroreflex control of the sympathetic nervous system.

1. In addition to its effects at the renal tubules to influence water retention and at vascular smooth muscle to cause vasoconstriction, the hormone arginine vasopressin also appears to modulate cardiovascular reflex control of the sympathetic nervous system. Infusion or endogenous release of vasopressin results in enhanced baroreflex sympatho-inhibitory responses compared with other pressor agents. In addition, when changes in arterial pressure are imposed on an elevated background level of circulating vasopressin, due either to infusion or endogenous release, the arterial baroreflex response is shifted to lower pressures, and the maximum sympatho-excitation to a decrease in pressure is reduced. 2. Evidence suggests that vasopressin may influence cardiovascular reflex function at multiple sites. Nevertheless, the primary site involved in the effects of circulating vasopressin on baroreflex function appears to be in the central nervous system, specifically in the area postrema. Lesion of the area postrema abolishes the ability of circulating vasopressin to modulate arterial baroreflex and cardiopulmonary reflex function and electrical or chemical stimulation of this circumventricular organ mimics the effects of vasopressin. In addition, vasopressin has been shown to influence the activity of area postrema neurons in vivo and in vitro. Although not all studies agree, the effects of the area postrema and vasopressin on cardiovascular reflex function appear to be dependent on afferent input from peripheral baroreceptors. 3. Most evidence suggests that vasopressin exerts its effects on baroreflex function through a V1 vasopressin receptor mechanism. Systemic administration or microinjection into the area postrema of a specific V1 receptor antagonist abolishes the action of arginine vasopressin on arterial baroreflex and cardiopulmonary reflex control of the sympathetic nervous system. 4. The ability of vasopressin and the area postrema to influence baroreflex function appears to be dependent on an alpha 2-adrenoceptor mechanism at the level of the nucleus tractus solitarius (NTS). Blockade of alpha 2-adrenoceptors in the NTS abolishes the effects of vasopressin and the area postrema on the sympathetic nervous system. Facilitation of NTS processing of baroreceptor afferent inputs by the area postrema could contribute to the enhanced sympatho-inhibition and shift of the baroreflex curve to lower pressures during elevations in circulating vasopressin.

Afferent Pathways↗
PubMed1996

Differential effects of reduced muscle use (hindlimb unweighting) on skeletal muscle with aging.

The changes in hindlimb muscle mass, fiber area and contractile tension that occurred with two weeks of reduced weight-bearing (HU) were of greater magnitude in 6-month-old as opposed to 36-month-old rats. The pattern of change following HU for young and old animals differed, which may indicate that multiple mechanisms are responsible for the observed changes. The majority of old rats had difficulty with ambulation following unweighting, suggesting that the functional consequences of reduced weight-bearing are greater in old than in young animals. One hour of weight-bearing during HU attenuated the decline in SOL fiber atrophy, muscle mass and Po, but had no apparent effect on the GAST, PL or EDL. The reduction in Po with HU was not due, except for the old PL, to changes at the neuromuscular junction.

Aging↗
PubMed1996

Complexity of age-related change in skeletal muscle.

Age-related changes in skeletal muscle mass, fiber area, and contractile function were examined in pathogen-free rats at 6, 12, 28 and 36 mos of age. The intent of this study was to clarify age-related decline, particularly in contractile force, and to determine if the decline in contractile tension with age is due to alterations at the neuromuscular junction. A variable amount of age-associated reduction in muscle mass was noted for the soleus (18%), extensor digitorum longus (EDL-16%), plantaris (37%), and gastrocnemius (38%) muscles. The decline in fiber area for these four muscles was between 5 and 16% greater than the loss in muscle wet weight. A variable amount of change in peak contractile force between 6 and 36 mos was observed for the soleus (62%), EDL (48%), and plantaris (34%). For soleus and EDL, the decline in peak tetanic tension exceeded the decline in muscle mass and fiber area. Most of the declines for the animals used in this study did not become significant until after the age of 28 mo. The marked reduction in peak tetanic tension, fiber area, and muscle mass between 28 and 36 mos indicates an accelerated age-related decline in this time period. The reduced peak twitch and peak tetanic tension in the oldest animals was not due to likely age-related changes at the neuromuscular junction. Peak values for tetanic tension were similar, whether tension was elicited via direct muscle stimulation or through stimulation of the nerve. Results underscore the complexity of age-related change and suggest that multiple mechanisms contribute to the decline of skeletal muscle.

Aging↗
PubMed1996

Acute and chronic angiotensin hypertension: neural and nonneural components, time course, and dose dependency.

We examined the mechanisms mediating hypertension in conscious rats during acute and chronic infusion of angiotensin II (ANG II) at pressor doses (50, 100, and 200 ng.kg-1.min-1). Trimethaphan-induced blood pressure reduction was inversely related to the acute dose of ANG II, consistent with a constrictor action of ANG II on vascular smooth muscle and withdrawal of sympathetic tone. During chronic ANG II infusion, the entire increase in mean arterial pressure (MAP) was inhibited by trimethaphan, consistent with neural mediation. During acute ANG II hypertension, the AT1-specific receptor blocker losartan induced a large fall in MAP (64 +/- 4 mmHg) in ganglion-blocked (chlorisondamine) rats, whereas, during chronic ANG II hypertension, losartan had only a small hypotensive effect (11 +/- 3 mmHg). To determine the time course of the change from vascular smooth muscle action to neural action, we measured MAP in response to trimethaphan during the first 24 h of ANG II infusion. After 5 h, the minimal MAP in response to trimethaphan was significantly higher than that before ANG II. After 10 h of infusion, trimethaphan decreased MAP to pre-ANG II levels. That is, the neural component was fully active after only 10 h of infusion in rats. Finally, chronic administration of ANG II resulted in a dose-related increase in MAP that, at all doses, was completely inhibited by trimethaphan. These findings are consistent with ANG II acting primarily on vascular smooth muscle during acute infusion and via neural pathways during chronic treatment. The transition from direct smooth muscle to indirect neural action is rapid in rats (< 10 h), and the MAP and neural responses to ANG II are dose related during chronic hypertension.

Acute Disease↗
PubMed1996

Area postrema voltage-activated calcium currents.

1. Calcium currents in rabbit area postrema neurons were studied with the perforated patch-clamp technique. Experimental conditions eliminated Na+ and K+ currents and identified both low- and high-threshold voltage-activated calcium currents. 2. Low-threshold, T-type calcium currents were observed in 64% of the area postrema neurons recorded. This current activated near -60 mV and had an average peak amplitude of -36.2 +/- 5 pA (mean +/- SE) at -40 mV. This current began rapid inactivation near -95 mV, reached half-maximal inactivation at -71 mV and was totally inactivated by -40 mV. 3. A high-threshold transient current was recorded in all area postrema neurons, which consisted of both a transient and sustained component. This current was present at voltages greater than -40 mV and the transient component of this current was responsible for the majority of the total Ca2+ current. 4. Nickel ions (10 microM) effectively reduced both the T-type current and the high-threshold current. Cadmium ions (100 microM) effectively reduced the high-threshold current while having insignificant effects on the low-threshold current. 5. Application of the dihydropyridine antagonist nimodipine (1-10 microM) had no effect on either the low- or high-threshold voltage-activated calcium Ca2+ in area postrema neurons. In addition, application of omega-conotoxin-GVIA (2-10 microM) was also without effect on either the low- or high-threshold voltage-activated Ca2+ current, suggesting that area postrema neurons possess neither L- or N-type voltage-activated Ca2+ currents. 6. Application of omega-conotoxin MVIIC (10 microM) significantly inhibited the peak high-threshold Ca2+ current by 65.4% suggesting that area postrema neurons do possess a omega-conotoxin MVIIC-sensitive high-threshold Ca2+ channel. 7. Arg-vasopressin (150 nM) significantly increased the transient component of the high-threshold Ca2+ current but had little effect on either the low-threshold or the high-threshold sustained component.

Angiotensin II↗
PubMed1995

Weight-bearing effects on skeletal muscle during and after simulated bed rest.

The detrimental consequences of bed rest include a rapid loss of muscle mass and strength. Yet, the utility of treatment to offset the effects of bed rest has not been well established. It was the purpose of this study to examine the effects of therapeutic intervention on simulated bed rest in rats. Simulated bed rest was accomplished by unweighting the hindlimbs of rats for 2 weeks via a suspension apparatus attached to the tail and midriff. Weight-bearing (eg, standing, walking) effects on hindlimb unweighting (HLU) were investigated under three conditions: (1) 1 hour of weight bearing per day during HLU; (2) a week of natural cage recovery after HLU; and (3) a combination of 1 hour of weight bearing per day during HLU and a week of recovery after HLU. Muscle contractile function and fiber atrophy were examined in the soleus (SOL), a postural muscle, and the extensor digitorum longus (EDL), a nonpostural muscle. The unweighted SOL showed a 37% loss in wet weight and a 61% decline in peak tetanic tension (P0). The SOL in rats allowed 1 hour of weight bearing per day lost 22% of its mass and 38% of its P0, a 38% attenuation. One week of cage recovery after HLU resulted in a SOL wet weight that was 26% less and P0 that was 42% less than controls. Animals that received the combination of 1 hour of weight bearing per day and 1 week of cage activity nearly recovered muscle mass, but P0 still was 19% less than controls. The EDL was much less affected by HLU than the SOL.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗
PubMed1995

Influence of nitric oxide on the hemodynamic response to hemorrhage in conscious rabbits.

We investigated the role of nitric oxide, an endothelium-derived relaxing factor, in the hemodynamic response to acute hemorrhage in conscious rabbits. Chronically instrumented rabbits were treated with the nitric oxide synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) or vehicle and hemorrhaged until mean arterial pressure fell below 40 mmHg. Control animals were treated with L-NAME or vehicle but not subjected to hemorrhage. L-NAME increased mean arterial pressure and decreased heart rate in control animals. Hindquarters and mesenteric blood flow velocity and conductance were reduced by L-NAME. Nitric oxide synthase inhibition also produced significant changes in the hemodynamic response to hypotensive hemorrhage. Mean arterial pressure was higher and regional vascular conductances were lower throughout hemorrhage and during recovery. L-NAME treatment significantly (but in some cases, subtly) altered the characteristic pattern of changes in vascular conductance associated with acute hypotensive hemorrhage and recovery. Similar experiments with other arginine analogues or phenylephrine infusion showed that L-NAME's effects during hemorrhage were due to nitric oxide synthase inhibition. We conclude that nitric oxide plays a role in the hemodynamic response to acute hemorrhage in the rabbit and is essential for the full expression of the vasodilation associated with hypotensive hemorrhage.

Amino Acid Oxidoreductases↗
PubMed1995

Rat aortic vasoreactivity is altered by old age and hindlimb unloading.

Prolonged bed rest in young adults leads to a number of cardiovascular alterations, including orthostatic intolerance and decreased exercise capacity. Similar changes occur with advanced age. These modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Using rat hindlimb unloading as an animal model of physical inactivity, this study was designed to determine whether prolonged decreases in weight-bearing activity induce changes in vascular reactivity that are similar to those occurring in senescent rats and whether the imposition of inactivity on old rats further modifies any age-related alterations in vasomotor responsiveness. Responses to vasoactive compounds were examined in vitro by using isolated abdominal aortic rings. Maximal isometric contractile force evoked by the vasoconstrictors KCl, norepinephrine (NE), and arginine vasopressin was lower in aortic segments from young hindlimb-unloaded (YHU), old control (OC), and old hindlimb-unloaded (OHU) rats compared with that from young control (YC) rats. Sensitivity [mean effective concentration (EC50)] to KCl was enhanced in segments from both old and unloaded animals compared with YC rats, but EC50 values for the other constrictors were not different among groups. Vasorelaxation responses induced by acetylcholine (10(-7) M NE preconstriction) were lower in vessel rings from OC (1 x 10(-7) to 3 x 10(-6) M), YHU (10(-7) to 10(-5) M), and OHU (10(-7) to 10(-5) M) rats than those from YC animals. In addition, vessel rings from OC, YHU, and OHU rats were less sensitive to sodium nitroprusside-induced relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Area postrema and aortic or vagal afferents converge to excite cells in nucleus tractus solitarius.

Area postrema neurons enhance baroreflex function, perhaps by augmenting baroreceptor afferent processing in the nucleus tractus solitarius (NTS). If so, NTS neurons should receive convergent excitatory inputs from area postrema neurons and baroreceptors. The aims of this study were to record extracellular activity of NTS neurons to determine whether 1) area postrema and aortic baroreceptor afferents converged in NTS, 2) area postrema and vagal afferents converged in NTS, and 3) the convergent inputs were facilitative. Studies were performed in pentobarbital sodium- or alpha-chloralose-anesthetized rabbits. Forty-six of 194 NTS neurons received inputs from the area postrema and aortic depressor nerve. Twelve of the 23 inputs showed facilitative summation; unit response rate evoked by paired inputs (79%) doubled the predicted (calculated) response rate for simple addition (37%). Fifty-eight of 114 NTS neurons received excitatory inputs from the area postrema and vagus. Eleven of the 13 inputs showed facilitative summation; unit response to paired inputs (87%) doubled the predicted response (44%). Area postrema neurons may augment the processing of aortic and vagal inputs by NTS neurons and, hence, enhance the reflex output of these afferent pathways.

Animals↗
PubMed1993

Role of alpha-adrenergic mechanisms on responses to area postrema stimulation and circulating vasopressin.

This study evaluated the role of catecholamines in the nucleus tractus solitarius (NTS) on the inhibition of renal sympathetic nerve activity (RSNA) due to direct electrical stimulation of the area postrema. In addition, the effects of catecholaminergic mechanisms in the NTS on the ability of circulating arginine vasopressin (AVP) to modulate arterial baroreflex control of RSNA were evaluated. Electrical stimulation of the area postrema (15 microA, 0.3 ms, 5-80 Hz) produced progressive decreases in RSNA. Responses to area postrema activation were not altered by microinjection of the alpha 1-adrenergic antagonist, prazosin, or vehicle bilaterally into the NTS. Microinjection of the alpha 2-antagonist, yohimbine (4 injections of 20-40 nl, 1 ng/nl), unilaterally into the NTS significantly attenuated the RSNA response to area postrema stimulation. Bilateral injection of yohimbine into the NTS abolished the response to area postrema activation (P < 0.05). Baroreflex inhibition of RSNA was significantly greater during infusion of AVP than during infusion of phenylephrine (slopes = -5.18 +/- 0.39 and -2.64 +/- 0.27 for AVP and phenylephrine, respectively). Microinjection of yohimbine bilaterally into the NTS did not alter the slope of baroreflex control of RSNA for phenylephrine but normalized the slope for AVP (-2.85 +/- 0.54) to that of phenylephrine. Data are consistent with the hypothesis that AVP effects on baroreflex inhibition of RSNA and area postrema-mediated inhibition of RSNA require alpha 2-adrenergic signaling within the NTS.

Adrenergic alpha-Antagonists↗
PubMed1993

Vasoconstrictor properties of rat aorta are diminished by hindlimb unweighting.

Prolonged bed rest and exposure to weightlessness in humans result in cardiovascular alterations that are characterized by orthostatic intolerance and decreased exercise capacity. Modifications of cardiovascular function have been suggested to be causally related to changes in peripheral vascular reactivity. Rat hindlimb unweighting (HU) was used as an animal model to determine whether prolonged decreases in weight-bearing activity induce changes in vasoreactivity of peripheral arterial vessels. Responses to vasoactive compounds were examined in vitro using isolated abdominal and thoracic aortic rings. Maximal isometric contractile tension evoked by the vasoconstrictors KCl (10-100 mM), norepinephrine (NE; 10(-9)-10(-4) M), phenylephrine (10(-9)-10(-4) M), arginine vasopressin (10(-13)-3 x 10(-5) M), and CaCl2 (10(-6)-10(-2) M) was lower in abdominal aortic rings from HU rats. Sensitivity [agonist concentration that produced 50% of maximal vasoconstrictor response (EC50)] to KCl was enhanced in segments from HU animals but was not different for the other constrictors. Maximal contractile responses of thoracic aortic rings to KCl (10-100 mM) and NE (10(-9)-10(-4) M) were also attenuated by HU. In abdominal aortic rings preconstricted with 10(-4) M NE, maximal vasodilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and 8-bromoguanosine 3',5'-cyclic monophosphate (10(-6)-10(-2) M) were greater in vessel rings from HU rats. However, with 10(-7) M NE preconstriction, maximal dilatory responses induced by sodium nitroprusside (10(-10)-10(-4) M) and acetylcholine (10(-9)-10(-4) M) were not different between groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Sympathoinhibition and its reversal by naloxone during hemorrhage.

During hemorrhagic hypotension, vascular resistance, plasma norepinephrine, and sympathetic nerve activity decrease. Naloxone reverses these effects. We hypothesized that increased sympathetic nerve activity was specific to naloxone and not secondary to the pressor response. Conscious rabbits were hemorrhaged until mean arterial pressure (MAP) was less than 40 mmHg, given naloxone (3 mg/kg) or saline, and monitored for 5 min. In some animals, we attenuated naloxone's pressor response with alpha-adrenergic blockade or mimicked the pressor response by infusion of phenylephrine. During nonhypotensive hemorrhage, heart rate and renal sympathetic nerve activity (RSNA) increased significantly. During hypotensive hemorrhage, RSNA decreased to significantly less than prehemorrhage control values. After saline treatment, RSNA did not increase. Naloxone significantly increased MAP and RSNA. alpha-Blockade reduced the pressor response to naloxone but not the increase in RSNA. Phenylephrine increased MAP to a level similar to naloxone, but RSNA remained suppressed. Reinfusion of hemorrhaged blood reduced RSNA in all groups treated with naloxone. These data suggest that hypotensive hemorrhage is associated with sympathoinhibition that is not transient. In addition, the pressor response to naloxone is not required for its sympathoexcitatory effects.

Analysis of Variance↗
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

Interaction of vasopressin and opioids during rapid hemorrhage in conscious rabbits.

We investigated possible interactions between arginine vasopressin (AVP) and endogenous opioid peptides during rapid hypotensive hemorrhage and subsequent opioid receptor blockade in conscious rabbits. Plasma AVP concentration did not change after normotensive hemorrhage but increased after hypotensive hemorrhage. Blockade of V1-AVP receptors (AVPX) did not affect prehemorrhage arterial pressure, heart rate, or hindquarter blood flow and vascular resistance. AVPX did not alter the hemodynamic response to hemorrhage or the blood loss required to reduce mean arterial pressure to less than 40 mmHg. However, hindquarter blood flow was higher and mean arterial pressure and hindquarter resistance lower after hypotensive hemorrhage in AVPX-treated animals. These differences were maintained after naloxone or saline injection. Naloxone increased mean arterial pressure and hindquarter resistance and decreased heart rate with or without AVPX. At 2 min postinjection, plasma AVP values were greater after saline than after naloxone. When naloxone's pressor response was reduced by alpha-adrenergic blockade, plasma AVP values were higher after naloxone than after saline. Thus AVP was not vital to maintenance of blood pressure during rapid normotensive hemorrhage or to the abrupt decrease in arterial blood pressure and resistance after rapid hypotensive hemorrhage. AVP release was important to spontaneous recovery from acute hypotensive hemorrhage but only of minor importance to naloxone's pressor response. Finally, AVP release appeared to be inhibited by endogenous opioids during acute hemorrhagic hypotension.

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↗
PubMed1989

Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release.

In conscious rats, intracerebroventricular (i.c.v.) injections of gamma-aminobutyric acid (GABA), a GABA-uptake inhibitor (nipecotic acid), and artificial CSF (aCSF) were restricted to forebrain regions and their effect on baroreceptor-mediated arginine-vasopressin (AVP) release was studied. AVP release was stimulated by the hypotension resulting from combined treatment with a converting enzyme inhibitor (CEI) and chlorisondamine (CHLOR), a ganglionic blocking agent. CEI + CHLOR reduced mean arterial pressure (MAP) from 118 +/- 2 to 63 +/- 2 mm Hg, but pressure then rose to a compensated level of 78 +/- 1 mm Hg. The compensation in MAP was shown to be AVP-dependent at the end of the experiment since the vascular AVP antagonist, d(CH2)5Tyr(Me)AVP, reduced MAP from 78 +/- 1 to 63 +/- 1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 micrograms) caused dose-related reductions in MAP (5 +/- 1.7 +/- 1 and 11 +/- 2 mm Hg, respectively). Nipecotic acid (3-350 micrograms) also caused dose-related reductions in MAP (from 3 +/- 1 to 15 +/- 2 mm Hg), while aCSF had no effect on MAP. Pretreatment with d(CH2)5Tyr(Me)AVP, antagonized completely the depressor effects of GABA and nipecotic acid. In other rats, blood samples were taken to measure the changes in plasma AVP concentrations (pAVP) induced by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 micrograms). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 +/- 8% reduction; P less than 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.

Animals↗
PubMed1989

The role of vasopressin in the pressor response to bilateral carotid occlusion.

Exogenous arginine vasopressin (AVP) has been shown to interact with the arterial baroreflex control of renal sympathetic nerve activity. In addition, we have shown that both AVP and the sympathetic nervous system (SNS) contribute to the pressor response to interruption of cardiopulmonary vagal afferents. This study examined the role and interaction of AVP and the SNS in the pressor response to a reduction of carotid sinus afferent activity by bilateral carotid occlusion (BCO). In addition the role of the area postrema (AP) in mediating the interaction between AVP and the SNS was examined. In aortic denervated conscious dogs, BCO increased mean arterial pressure 51.7 +/- 3.1 mm Hg. Specific vascular (V1) AVP antagonist D(CH2)5Tyr(Me)AVP did not alter the response to BCO (delta 50.8 +/- 7.9 mm Hg). Subsequent ganglionic blockade abolished the response to BCO (delta -10 +/- 3.8). When ganglionic blockade was induced in the absence of AVP antagonist, BCO increased MAP 25.0 +/- 2.8 mm Hg. AVP antagonist following ganglionic blockade eliminated the pressor response to BCO (delta -6.7 +/- 5.1). There was an interaction between AVP and the SNS such that the contribution of one system to the hemodynamic response was greater in the absence of the other system. Ablation of the AP abolished the interaction between reflexly released AVP and the SNS which was observed in intact dogs. These data demonstrate that both AVP and the SNS contribute to the pressor response to BCO. Reflexly released AVP appears to limit the reflex activation of the SNS. The interaction of endogenous AVP and the arterial baroreflex involves the AP. The results are consistent with the hypothesis that vasopressin interacts centrally to limit a reflex increase in sympathetic outflow and thus modulate the pressor response to BCO.

Adrenergic Fibers↗