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PubMed2002

[Phytoestrogen genistein inhibits carotid sinus baroreflex in anesthetized male rats].

The purpose of this study was to determine the effect of phytoestrogen genistein (GST) on carotid sinus baroreflex in 30 anesthetized male rats by perfusing the isolated carotid sinus in vivo. The results obtained are as follows. (1) By perfusion with GST (50 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a peak slope (PS) decrease from 0.36+/-0.01 to 0.23+/-0.01 (P<0.001) and a reflex decrease (RD) in mean arterial pressure from 39.75+/-1.58 to 27.00+/-0.60 mmHg (P<0.001), while the threshold pressure (TP) and saturation pressure (SP) were significantly increased from 65.63+/-2.1 to 82.05+/-1.95 mmHg (P<0.001) and from 192.23+/-3.90 to 215.76+/-3.75 mmHg (P<0.001), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with Bay K 8644 (500 nmol/L), an agonist of calcium channels, could completely abolish the inhibitory effect of GST on carotid baroreflex. (3) Preperfusion with an inhibitor of NO synthase, L-NAME (100 micromol/L), did not affect the inhibitory effect of GST. It is proposed that the inhibitory action of GST on carotid baroreflex may be mediated by the inhibition of Ca(2+) channel of vascular smooth muscle, but not by NO release from endothelium.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2002

Deterioration in carotid baroreflex during carotid endarterectomy.

OBJECTIVE: Blood pressure instability after carotid endarterectomy (CEA) has been associated with a disturbance of the baroreflex control mechanism caused by the surgery in the carotid sinus region. The purpose of this study was to determine if a deterioration in carotid baroreceptors occurs during the surgery. METHOD: Heart rate (HR) and blood pressure (BP) were recorded continuously in 60 patients undergoing CEA as well as preoperatively and postoperatively at 2 days and 6 weeks. The baroreflex sensitivity was determined by cross-spectral analysis of HR and systolic blood pressure (SBP). During the surgery, three tests were used to assess the baroreflex response. The first test simulated a sudden fall in systemic blood pressure by clamping the common carotid artery. The second test simulated a rise in systemic blood pressure by applying pressure by using a rubbing action on the luminal surface of the carotid sinus region. The rub test was performed twice, once with the atheromatous plaque in situ and once when the plaque had been removed. The third test is clamp removal and restoration of blood flow through the carotid sinus. RESULTS: Carotid cross-clamping increased mean +/- standard error of the mean SBP from 117 +/- 3 mm Hg before clamping to 125 +/- 3 mm Hg (P <.05) at 30 beats after clamping. The first rub test with the plaque in situ decreased SBP from 121 +/- 3 mm Hg to 117 +/- 3 mm Hg (P <.01) at 10 beats after the rub test, indicating a functioning baroreceptor reflex. The second rub test increased SBP from 126 +/- 3 mm Hg to 128 +/- 3 mm Hg (P <.05). SBP dropped (P <.01) when unclamping suggesting a selective alteration of the baroreflex sensitivity. The baroreflex sensitivity was significantly reduced 2 days postoperatively when compared to preoperative values (P <.05). CONCLUSIONS: These findings suggest that the act of plaque removal could be associated with a partial disruption of baroreceptor mechanism in the carotid artery. This could affect type I baroreceptors.

Aged↗
PubMed2003

Baroreflex function in vasodepressive syncope: detection of early impairment.

BACKGROUND: Defective baroreflex function has been suggested as a potential mechanism accounting for the development of syncopal episodes. The present study was therefore aimed at assessing the non-invasive, indirect hemodynamic profile and baroreflex function by means of tilting, which is a natural stimulation crucial to physiological baroreflex activity, in syncopal patients and healthy controls. MATERIAL/METHODS: Seventeen consecutive patients with a positive response to head-up tilting and fourteen healthy subjects as controls underwent continuous and non-invasive beat-to-beat heart rate and arterial pressure measurements in order to evaluate systolic, diastolic, and dicrotic pressures, as well as heart rate. Baroreflex function was calculated as the slope of the linear regression line relating systolic arterial pressure to RR interval changes during upward and downward phases of tilting, respectively. RESULTS: When compared to healthy subjects, vasodepressive patients showed a significantly weaker correlation between systolic pressure and RR interval changes both in upward tilting, (r = 0.68 vs r = 0.91, p<0.05) and downward tilting (r = 0.48 vs r = 0.93, p<0.01). CONCLUSIONS: Our results show that an impairment in baroreflex-mediated adjustment to postural challenge can be detected in syncopal patients also during upward tilting, that is, in the early phase of the test. Moreover, our investigation emphases the utility of a noninvasive, complete hemodynamic evaluation of the early phase of tilting in order to detect peculiar behaviours of pulse wave contour and related parameters.

Adult↗
PubMed1994

Changes in spontaneous baroreflex sensitivity during sleep in humans.

To evaluate changes in the spontaneous baroreflex sensitivity for heart rate and for muscle sympathetic nerve activity (MSNA) during sleep, we simultaneously recorded MSNA from the tibial nerve and monitored ECG, EEG, EOG, EMG and blood pressure during the resting awake stage and sleep. Blood pressure, ECG and MSNA waves were changed to equidistant time series data of each second by cubic spline interpolation. Cross correlations between the MSNA and diastolic blood pressure and between the instantaneous heart rate and systolic blood pressure were analyzed. Spontaneous baroreflex sensitivities for MSNA and for heart rate were assessed from the slope of the regression lines for each. During sleep, the spontaneous baroreflex sensitivity for MSNA gradually decreased as the non-REM sleep stages advanced. Spontaneous baroreflex sensitivity for heart rate did not show any apparent changes. These results suggest that baroreflex modulations for heart rate and for MSNA differ during sleep.

Adult↗
PubMed2002

Effects of prolonged bed rest on the total peripheral resistance baroreflex.

Orthostatic intolerance following prolonged exposure to microgravity continues to be a primary concern of the human space program. Reduced autonomic tone has been demonstrated to contribute to this phenomenon, and the heart rate baroreflex, in particular, has been repeatedly shown to be impaired. However, only the works of Yelle et al. have attempted to address the role of the total peripheral resistance (TPR) baroreflex, a potentially more significant contributor to blood pressure regulation. We applied a previously developed method for estimating the static gains of both the arterial and cardiopulmonary TPR baroreflexes to data obtained before and after 16-day bed rest. Reductions in the estimated static gains of the arterial (statistically significant) and cardiopulmonary TPR baroreflexes were found after bed rest. This study supports the works of Yelle et al, which imply that the TPR baroreflex is reduced after spaceflight.

Adult↗
PubMed2004

Cholecystokinin octapeptide inhibits carotid sinus baroreflex in anesthetized rats.

The purpose of this study was to determine the effect of cholecystokinin octapeptide (CCK-8) on carotid sinus baroreflex in 36 anesthetized male rats by isolated carotid sinus perfusion in vivo. The results obtained are as follows. (1) By perfusion with CCK-8 (0.1, 0.5, 1.0 micromol/L), the functional curve of baroreflex was shifted to the right and upward, with a decrease in peak slope (PS) (p<0.001) and a reflex decrease (RD) in mean arterial pressure, while the threshold pressure (TP) and saturation pressure (SP) were significantly increased. Among the functional parameters of carotid sinus baroreflex, the changes in RD, PS and TP were dose-dependent. (2) Pretreatment with proglumide (100 micromol/L), a nonselective CCK receptor antagonist, the inhibitory effect of CCK-8 (0.5 micromol/L) on the baroreflex was significantly attenuated. (3) Pretreatment with L-NAME (100 micromol/L), an inhibitor of nitric oxide (NO) synthase, did not affect the inhibitory action of CCK-8 (0.5 micromol/L). (4) Preperfusion with Bay K 8644 (500 nmol/L), an agonist of calcium channel, could attenuate the effect of CCK-8 (0.5 micromol/L). It is suggested that the inhibitory action of CCK-8 on the baroreflex may be mediated by the activation of its receptors in the carotid sinus baroreceptor, leading to an inhibition of stretch-sensitive channels and a decrease in Ca(2+) influx. However, NO released from the endothelium seems not to be involved in the mechanism of this effect.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed2005

[Effect of microinjection of atrial natriuretic peptide into the paraventricular nucleus on baroreflex sensitivity in conscious rats].

The role of atrial natriuretic peptide (ANP) in the central regulation of the circulation is known to be a neurotransmitter or a neuromodulator, but its actions on baroreceptor reflex function are not fully resolved. The present study examined the role of ANP (6, 60 ng/0.2 microl) by direct microinjection into the hypothalamic paraventricular nucleus (PVN) in conscious rats. OPC-21268 (0.45 microg/3 microl), an antagonist of the V(1) receptor, was microinjected into the lateral ventricle to examine whether the effect of ANP on baroreflex sensitivity is mediated by vasopressin (VP). ANP significantly increased the baroreflex sensitivity, and OPC-21268 attenuated the increase of baroreflex sensitivity induced by ANP. Intravenous injections of ANP (60 ng/0.04 ml) did not affect baroreflex sensitivity. These results suggest that ANP in the PVN may produce a facilitative effect on baroreflex, and the effect may be via, at least in part, the central vasopressin.

Animals↗
PubMed1995

[Baroreflexes and congestive heart failure].

Abnormal responses are found in the early stages of heart failure with increased sympathetic and decreased parasympathetic activity, causing peripheral arteriolar vasconstriction and tachycardia respectively. The cardiopulmonary baroreflex may be studied by decreasing venous return ("low body negative pressure") and by measuring vascular resistance forearm. The arterial baroreflex may be studied by changing aortic pressures (by intravenous phenylephrine or nitroglycerin). Orthostatism and the tilt test deactivate the cardiopulmonary and arterial baroreflexes simultaneously. These baroreflexes are impaired in patients with heart failure. Their activation does not cause the usual sympatho-inhibition so contributing to increased sympathetic tone. This dysfunction may result from a change at any point on the reflex pathway: the baroreceptors themselves, the afferent, central and efferent pathways. It is selective as during the cold pressor test, the vasoconstrictor response remains intact. One of the possible mechanisms of baroreflex dysfunction in heart failure is loss of sensitivities of the baroreceptors. This may be multifactorial: structural abnormalities, changes in compliance or functional abnormality. Even if the loss of sensitivity is partially related to a change in compliance, other factors play a role. It is more functional than structural abnormalities because, after cardiac transplantation, the baroreceptors regain their sensitivity within 2 to 3 weeks. Excessive Na-K dependent ATPase activation of the smooth muscle cells of the carotid sinus could lead to hyperpolarization of the cell membrane, so reducing the excitability of the receptor. Aldosterone is one of the factors which could activate the Na-K ATPase, as this hormone directly increases pump activity and favorizes the synthesis of new pumps in the vascular smooth muscle cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Autonomic Nervous System↗
PubMed1995

Effect of acute and chronic treatment with the angiotensin II subtype 1 receptor antagonist EXP 3174 on baroreflex function in conscious spontaneously hypertensive rats.

OBJECTIVE: To determine whether the angiotensin II subtype 1 (AT1) receptor antagonist EXP 3174 can modify the baroreceptor-heart rate reflex in conscious rats. DESIGN: EXP 3174 was given acutely, both peripherally and centrally, as well as chronically to spontaneously hypertensive rats (SHR), and baroreflex function was then examined. METHODS: Baroreceptor reflex activity was assessed by constructing sigmoidal mean arterial pressure (MAP)-heart rate curves after injection of pressor (phenylephrine) and depressor (sodium nitroprusside) agents. Baroreflex testing was performed before and after intravenous (1 mg/kg) and intracerebroventricular (1 microgram) administration of EXP 3174 in separate groups of conscious SHR and Wistar-Kyoto (WKY) rats. EXP 3174 was also given subcutaneously for 15 days (5 mg/kg per day) in SHR, and baroreceptor reflex activity was assessed approximately 24 h later. RESULTS: EXP 3174 lowered MAP after acute peripheral administration in SHR and, to a lesser extent, WKY rats. MAP was not altered after central administration of EXP 3174 in either group. Baroreceptor reflex function was not significantly modified after acute peripheral or central injection of the AT1 receptor antagonist in SHR or WKY rats. In contrast, chronic treatment of SHR with EXP 3174 markedly decreased MAP compared with vehicle-treated SHR. Moreover, the MAP-heart rate curve was shifted leftwards together with an enhancement of reflex bradycardia, such that baroreflex function was restored to the level observed in untreated WKY rats. CONCLUSION: Chronic, but not acute, administration of EXP 3174 normalized baroreflex function in SHR. This facilitation of baroreflex function might contribute to the greater antihypertensive effect observed after chronic administration of EXP 3174 in SHR.

Angiotensin Receptor Antagonists↗
PubMed1995

The effect of hypoxia on baroreflexes and pressor sensitivity in sleep apnea and hypertension.

Many persons with sleep apnea are hypertensive. Forty-two subjects of similar age and weight were divided into four groups of hypertensives and normotensives with and without sleep apnea. All subjects had heart rate, blood pressure (BP), baroreflex sensitivity and pressor sensitivity to phenylephrine measured while breathing room air or 15% oxygen. Hypoxia raised heart rate and lowered BP in all groups (p < 0.001), with the greatest hypotensive effect among hypertensives. Hypertensives had blunted baroreflex sensitivity, and breathing a hypoxic mixture lowered baroreflex sensitivity of all four groups (p = 0.008). The apneic subjects tended to lower their baroreflex sensitivity more in response to hypoxia and also had an enhanced pressor response to phenylephrine, whether breathing room air or 15% oxygen. Episodes of sleep apnea lead to hypoxia, an initial period of hypotension and a subsequent increase in sympathetic nervous activity. Our studies suggest that apneics could have an exaggerated pressor sensitivity to norepinephrine. They might also have difficulty returning BP to normal levels, because hypoxia impaired baroreflexes.

Adult↗
PubMed1997

Limited utility of the phenylephrine-nitroprusside sigmoid curve method of measuring baroreflex function after myocardial infarction.

BACKGROUND: Conventional testing of baroreflex function with phenylephrine bolus injection measures reflex vagal tone. OBJECTIVE: To evaluate an alternative pharmacological method of baroreflex testing, which might provide more comprehensive evaluation of the baroreflex function in patients with uncomplicated myocardial infarction. METHODS: Forty-eight patients, aged 59 +/- 7 years, were evaluated 5-7 days after myocardial infarction and after 6 weeks of rehabilitation. Baroreflex testing was performed with 10-14 incremental injections of nitroprusside and phenylephrine. The peak heart rate and blood pressure point from each injection were fitted to a four parameter (upper plateau, lower plateau, gain and median blood pressure) sigmoid logistic function. The baroreflex sensitivity (BRS) was also measured by conventional linear analysis of the response of the R-R interval to the initial rise in systolic blood pressure induced by phenylephrine bolus injection. RESULTS: Non-linear curve fitting of four logistic curve parameters was possible for results from 91% of tests; in the remaining tests the upper plateau was held constant at the maximum heart-rate response to allow estimation of the other three parameters. When all four parameters had been estimated, the gain parameter could not be precisely determined (the coefficient of variation of the gain parameter was 85 +/- 10%). The upper (R = 0.72, P < 0.001) and lower plateaux (R = 0.76, P < 0.001) were strongly related to the resting heart rate and weakly related to measures of heart-rate variability. There was also a significant inverse correlation between the lower plateau and the BRS (R = -0.57, P < 0.001). The gain parameter was not related to the BRS or any measure of the heart-rate variability. After 6 weeks' rehabilitation there was a significant decrease in the lower plateau (from 54 +/- 2 to 48 +/- 1 beats/min, P < 0.001), an increase in BRS (from 9.4 +/- 0.8 to 12.1 +/- 0.8 ms/mmHg, P < 0.001) and no change in the other three sigmoid curve parameters. CONCLUSIONS: Non-linear curve fitting of the heart-rate-blood-pressure relationship for patients after myocardial infarction is feasible but technical limitations and the lack of correlation between the gain parameter and other measures of autonomic function suggest that this method has limited usefulness. The lower plateau is related strongly to the BRS; both are vagal measures of cardiac autonomic function.

Aged↗
PubMed1998

Attenuation of cardiac but not vascular component in baroreflex of spontaneously hypertensive rats.

The cardiac and vascular components of the baroreceptor reflex in spontaneously hypertensive rat (SHR) and stroke-prone spontaneously hypertensive rat (SHRSP) were compared against their counterparts in normotensive Wistar Kyoto rat (WKY). SHR, SHRSP and WKY of 12-16 weeks old were chronically instrumented for intra-arterial recording of blood pressure. Intravenous injections of phenylephrine and nitroprusside were used to challenge their baroreflex. The products of blood pressure change and the half time required for the pressure to return to the control value were used as the quantitative estimation of the blood pressure stabilizing capability. The cardiac component of the baroreflex was obtained from the change in the blood pressure stabilizing capability after blockade of beta and muscarinic receptors by atenolol and atropine, respectively. The vascular component was obtained by subtracting the cardiac component from the total stabilizing capability which was the difference after blockade with a ganglionic transmission blocker, hexamethonium. We found the cardiac component of the baroreflex of the hypertensive rats was significantly less sensitive than that of the WKY. In contrast, the vascular component of the baroreflex of the three strains did not differ significantly. Therefore, we concluded that the 12-16 week old SHRs were able to maintain a stable blood pressure due to the intact vascular component of the baroreflex.

Adrenergic alpha-Agonists↗
PubMed1977

Baroreflex sensitivity during operant blood pressure conditioning.

Baroreflex sensitivity was measured in baboons operantly conditioned to increase their diastolic blood pressure in daily, 12-hr sessions, by using the extent of increases in interpulse interval per unit of increase in systolic pressure after intravenous phenylephrine injection as an index of baroreflex sensitivity. Following training, baroreflex sensitivity increases averaging 32% were observed before and after the 12-hr conditioning sessions. During the conditioning sessions, however, consistent diastolic blood pressure elevations averaging 17% (14 mmHg) were accompanied by significant decreases in baroreflex sensitivity averaging 44% relative to the increased "before" and "after" sensitivity levels. The results suggest that changes in baroreflex sensitivity participate in operantly conditioned blood pressure changes.

Animals↗
PubMed1992

Arterial baroreflex attenuation during and after continuous propofol infusion.

The reduction of arterial blood pressure produced by propofol may be, in part, attributable to impaired baroreflex integrity. The purpose of this study was to investigate arterial baroreflex sensitivity during and after continuous propofol infusion. In urethane anaesthetized rabbits, left renal sympathetic nerves were exposed and placed on a bipolar silver electrode to record renal sympathetic nerve activity (RSNA). Mean arterial pressure (MAP) via a femoral artery and heart rate (HR) by electrocardiogram were continuously recorded. The rabbits were divided into two groups of eight each: Group 1, propofol 5 mg.kg-1 bolus followed by infusion 0.5 mg.kg-1 x min-1; Group 2, propofol 2 mg.kg-1 bolus followed by 0.2 mg.kg-1 x min-1. Phenylephrine pressor and sodium nitroprusside (SNP) depressor tests were carried out before propofol was started (control), at 15 and 30 min during 30 min infusion, and at 15, 30 and 60 min after its discontinuation. The change of RSNA was plotted with respect to every 5 mmHg increment and decrement of MAP to construct sympathetic baroreflex sigmoid curves, and to evaluate baroreflex sensitivity. The baroreflex sensitivity was also evaluated by calculating the ratio of maximum increase of RSNA or HR to SNP-induced maximum decrease of MAP (delta RSNA/delta MAP, delta HR/delta MAP). Despite the same decreases or increases in MAP, RSNA was attenuated after 15 and 30 min of propofol infusion in both groups compared with control (P < 0.05). Decreased delta RSNA/delta MAP gradually returned to the control level 60 min after discontinuation of propofol in Group 1.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Influence of nifedipine on arterial baroreflex modulation of heart rate control during dynamic increases in arterial pressure: studies in normal man.

Studies in animals have demonstrated that calcium channel blocking agents exert important influences on autonomic mechanisms in addition to their direct vascular effects. Previous studies in our laboratory showed that clinical doses of nifedipine sensitized baroreceptor-mediated control of peripheral vascular resistance in normal human subjects. However, baroreflex control of vascular tone does not necessarily imply parallel control of heart rate. A series of experiments was therefore performed to test the hypothesis that therapeutic doses of nifedipine would potentiate arterial baroreflex modulation of heart rate during ramp increases of arterial pressure in normal volunteers. Arterial baroreflex control was assessed by measuring heart interval (HI) responses to dynamic ramp elevation of systolic arterial pressure (SAP) with bolus administration of phenylephrine (PE) before and after nifedipine or placebo in 19 normal subjects. Arterial baroreflex control was calculated from the slope of the regression of SAP on succeeding HI during the first 18 cardiac cycles following onset of rise of SAP after PE bolus. In 13 subjects, bolus PE produced an increase in SAP from 125 +/- 3 mm Hg to 152 +/- 5 mm Hg (p less than 0.01), with a resultant increase in HI from 1110 +/- 57 msec to 1541 +/- 87 msec (p less than 0.01). The baroreflex response was linear (r greater than 0.80, p less than 0.025) and = 17.8 +/- 3.3 msec/mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

Effects of heart failure on baroreflex control of sympathetic neural activity.

Baroreflex control of heart rate, vascular resistance and norepinephrine is impaired in patients with heart failure, but recent animal studies demonstrate preserved baroreflex control of sympathetic nerve activity in this disorder. Studies were therefore performed to compare baroreflex control of efferent sympathetic nerve activity to muscle in 10 normal subjects (age mean +/- SEM 21 +/- 1 years) and in 11 patients with moderate to severe heart failure (age 48 +/- 5 years, New York Heart Association class II to IV, left ventricular ejection fraction 19 +/- 2%, pulmonary capillary wedge pressure 27 +/- 2 mm Hg, cardiac index 2.04 +/- 0.22 liters/min/m2). Baroreflex activation was produced by intravenous infusion of phenylephrine (0.5 to 2.0 micrograms/kg/min) and deactivation by infusion of nitroprusside (0.4 to 2.5 micrograms/kg/min). During phenylephrine infusion, comparable increases in mean arterial pressure were produced in normal subjects (89 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01) and in patients with heart failure (90 +/- 2 to 99 +/- 3 mm Hg, p less than 0.01). The patients with heart failure exhibited significantly attenuated (p less than 0.01 for normal vs heart failure) decreases in heart rate (93 +/- 5 to 90 +/- 6 beats/min, p = not significant [NS]) compared with normal subjects (67 +/- 3 to 58 +/- 4 beats/min, p less than 0.01) and tended to demonstrate attenuated sympathoinhibitory responses to this pressor stimulus. More strikingly, patients with heart failure demonstrated significant impairment of baroreflex responses during nitroprusside-induced baroreceptor deactivation. In normal subjects, nitroprusside produced a decrease in mean arterial (90 +/- 2 to 80 +/- 3 mm Hg, p less than 0.001) and right atrial (4 +/- 1 to 2 +/- 1 mm Hg, p less than 0.01) pressures with a resultant reflex increase in heart rate (68 +/- 3 to 81 +/- 4 beats/min, p less than 0.001) and muscle sympathetic nerve activity (326 +/- 74 to 746 +/- 147 U/min, p less than 0.01). In patients with heart failure (n = 10), nitroprusside produced comparable (p = NS for normal vs heart failure) decreases in mean arterial (89 +/- 2 to 77 +/- 2 mm Hg, p less than 0.001) and right atrial (6 +/- 1 to 1 +/- 1 mm Hg, p less than 0.001) pressures, but did not significantly alter heart rate (91 +/- 6 to 97 +/- 4 beats/min, p = NS) or sympathetic nerve activity (936 +/- 155 to 1179 +/- 275 U/min, p = NS).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1992

Inhibition of baroreflex bradycardia by ethanol involves both GABAA and GABAB receptors in the brainstem of the rat.

The effects of ethanol on baroreceptor reflex bradycardia and its interactions with cardiovascular effects mediated by GABA receptors in the dorsal vagal complex were studied in urethane-anaesthetised rats. Ethanol, 1 g kg-1 administered i.v. or 25-200 nmol microinjected bilaterally into the dorsal vagal complex, inhibited the reflex bradycardic response to bolus i.v. doses of phenylephrine both in spontaneously breathing and in paralysed, artificially ventilated animals, and this effect could be prevented by pretreatment with the GABA-depleting agent, 3-mercaptopropionate in both groups of rats. Ethanol, 1 g kg-1 i.v., did not influence the bradycardic response to electrical stimulation of the cervical vagus. Microinjection of muscimol into the dorsal vagal complex caused a dose-dependent pressor response and inhibited baroreflex bradycardia. The pressor response was potentiated and a tachycardic response to muscimol emerged following microinjection of ethanol into the dorsal vagal complex. Similar administration of baclofen caused dose-dependent increases in blood pressure and heart rate and inhibited baroreflex bradycardia. Injection of ethanol into the dorsal vagal complex potentiated the pressor response to a low dose of baclofen but did not affect the tachycardic response. Bicuculline, 10 pmol/side into the dorsal vagal complex, blocked the effects of muscimol but not those of baclofen and reduced the baroreflex inhibitory action of ethanol. 2-Hydroxysaclofen, microinjected at 400 pmol to 1 nmol/side, blocked the effects of baclofen but not those of muscimol. 2-Hydroxysaclofen or phaclofen, 2 mg kg-1 s.c., prevented the baroreflex inhibitory action of ethanol and also prevented ethanol potentiation of the pressor and, less effectively, the tachycardic effects of muscimol. It is concluded that ethanol inhibits baroreflex bradycardia through potentiation of the actions of endogenous GABA in the dorsal vagal complex. Both GABAA and GABAB receptors appear to be involved in this action of ethanol.

3-Mercaptopropionic Acid↗
PubMed1988

Role of baroreflex in the pressor response of rats with hypertension developed by renal artery stenosis.

We examined the interrelationships between the pressor response to the administration of norepinephrine and arginine vasopressin and baroreflex function in rats with hypertension of two days' duration induced by heminephrectomy and a clip placed on the right renal artery (2-day clipped rats). Mean arterial pressure was higher in the 2-day clipped rats than in heminephrectomized rats without clips (sham-operated rats). The pressor response in the 2-day clipped rats to both agents increased as compared to the sham-operated rats. This hyperresponsiveness was attenuated by administering an angiotensin II antagonist, [1-Sar, 8-Ile] angiotensin II. Baroreflex sensitivity was studied by measuring changes in arterial pressure and pulse interval in response to the injection of phenylephrine. Baroreflex sensitivity was not decreased but markedly increased in the 2-day clipped rats and unaffected by infusing the angiotensin II antagonist. These results provide evidence that 1) in the 2-day clipped rats there are exaggerated pressor responses to vasoconstrictors; 2) the hyperresponsiveness is not causally related to the change of baroreflex sensitivity; and 3) angiotensin II plays a significant role in the increased pressor responses; however, the baroreflex mechanism is not involved in attenuation of the hyperresponsiveness by the angiotensin II antagonist.

1-Sarcosine-8-Isoleucine Angiotensin II↗