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PubMed1985

Baroreflex function and pressor responsiveness in normotensive young subjects with a family history of hypertension.

Baroreflex control of heart rate, pressor responses to alpha agonist (phenylephrine) and isometric exercise before and during salt loading were compared between 13 normotensive subjects with hypertensive relatives (group A) and 9 normotensive subjects with no family history of hypertension (group B). Baroreflex slope was significantly lower in group A than in group B (9.6 +/- 1.6 vs 17.6 +/- 1.9 msec/mmHg; p less than 0.01), although blood pressure, heart rate and aortic distensibility were not different between two groups. Pressor responses to phenylephrine and isometric exercise were identical for both groups. During salt loading, pressor responses to phenylephrine and isometric exercise were significantly greater in group A than in group B. Baroreflex slope was not affected by salt loading in the two groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated arterial pressure and decreased aortic distensibility. Pressor responses to alpha agonist and isometric exercise during high-sodium diet were augmented in subjects with a family history of hypertension.

Adult↗

PubMed1992

Difference between halothane and barbiturate anesthesia in the influence of cerebral ischemia on the vagal baroreflex in dogs.

In halothane-anesthetized dogs, a decrease in baroreflex sensitivity (BRS) of approximately 20% was observed during the reperfusion period following 5-min global cerebral ischemia. When compared with our previous study on animals under pentobarbital anesthesia, the extent of the decrease in BRS was smaller and apparently more severe ischemia was necessary to damage the vagal component of the baroreflex. Substitution of halothane with pentobarbital during the reperfusion period failed to affect either BRS or the ratio of the vagal component. In another group, pre- and post-ischemic measurements of BRS was performed under halothane anesthesia, but the ischemic insult was given under thiopental anesthesia. In these animals, the extent of decrease in BRS (about 50%) was greater than that in animals subjected to ischemia under halothane anesthesia. The present results suggest that the anesthetics used during the ischemic insult may affect the extent of post-ischemic dysfunction of the baroreflex. The vagal component of the baroreflex may be more resistant to ischemia under halothane anesthesia than under barbiturate anesthesia.

Anesthesia↗

PubMed1988

Interference of ketanserin with baroreflex control of the circulation in the conscious spontaneously hypertensive rat.

Ketanserin suppresses baroreflex-mediated tachycardia following the administration of hypotensive doses of sodium nitroprusside in conscious spontaneously hypertensive rats (SHR). The purpose of this study was to compare the baroreflex effects of ketanserin with those of the more selective S2-serotonergic receptor antagonist ritanserin and the alpha 1-blocker prazosin. In conscious SHR, both ketanserin (3 mg/kg) and prazosin (0.01 and 0.1 mg/kg) caused a significant reduction in blood pressure. Ritanserin (3 mg/kg) and the combination of a low dose of prazosin (0.01 mg/kg) and ritanserin (3 mg/kg) did not lower blood pressure significantly. Baroreflex responses were determined by measuring the maximal changes in heart period (HP = 60,000/HR) after administration of 20 to 100 micrograms/kg sodium nitroprusside. Whereas saline and prazosin lacked an effect on changes in HPmax, ketanserin reversed the decrease in delta HPmax into a significant increase. Ritanserin alone caused a slight but insignificant inhibition, whereas the combination of ritanserin and prazosin blocked the sodium nitroprusside-induced reflex tachycardia. Ritanserin, in contrast to prazosin or ketanserin, lowered resting heart rate values. We conclude that the interference of ketanserin with the baroreflex in SHR is a unique property of this agent, related to its simultaneous effects on serotonin (5-HT) S2-receptors and alpha 1-adrenoceptors.

Animals↗

PubMed1980

Baroreflex sensitivity in rabbits during the development of experimental renal hypertension and medial sclerosis.

Baroreflex sensitivity was assessed in 9 normotensive (N), 8 renal wrap (one kidney model, RH) and 16 medial sclerotic rabbits (MS, fed on calciferol 50,000 i.u. and calcium lactate 1g for 10 days) before (mean BP;N, 79 +/- 3.3 mm Hg; RH, 80 +/- 7.4 mm Hg; and MS, 83 +/- 1.0 mm Hg) and at monthly intervals for up to 16 weeks after the induction of the disease processes (mean BP;N, 87 +/- 3.9 mm Hg; RH, 127 +/- 7.2 mm Hg and MS, 99 +/- 3.8 mm Hg). Blood pressure was elevated by i.v. phenylephrine (5 and 10 micrograms.kg-1) or angiotensin (250 ng.kg-1) and baroreflex sensitivity assessed by the increase of pulse interval per unit rise of pressure. The pressor response was greater in the RH and MS than in the N rabbits. The baroreflex sensitivity showed a progressive reduction with time and with the elevation of blood pressure in both MS and RH rabbits. The difference was significantly greater (P < 0.01) than in the aged related control rabbits (P < 0.05). There was an inverse relationship between baroreflex sensitivity and the pressor response in MS rabbits. Results indicated progressive baroreceptors dysfunction in hypertensive and medial sclerotic rabbits.

Angiotensin II↗

PubMed1999

Gender difference in baroreflex-mediated bradycardia in young rats: role of cardiac sympathetic and parasympathetic components.

In a previous clinical study we have demonstrated a significantly lower baroreflex-mediated bradycardic response in young women compared with men. The present study determined whether sexual dimorphism in baroreflex sensitivity in young rats also covers the reflex tachycardic response. The study was then extended to test the hypothesis that an attenuated cardiac cholinergic component of the baroreflex heart rate response in females may account for the gender difference. Baroreflex sensitivity (BRS) was expressed as the regression coefficient of the reciprocal relationship between evoked changes in blood pressure and heart rate. BRS measured in conscious rats with phenylephrine (BRS(PE)) and nitroprusside (BRS(NP)) represented the reflex bradycardic and tachycardic responses, respectively. Female rats exhibited significantly lower BRS(PE) compared with male rats (-1.53+/-0.1 vs. -2.36+/-0.13 beats x min(-1) x mmHg(-1); p < 0.05) but similar BRS(NP) (-2.60+/-0.20 vs. -2.29+/-0.17 beats x min(-1) x mmHg(-1)). Blockade of cardiac muscarinic receptors with atropine methyl bromide elicited greater attenuation of BRS(PE) in male than in female rats (72+/-4.6 vs. 53+/-6.7% inhibition; p < 0.01) and abolished the gender difference. In male rats cardiac muscarinic blockade attenuated BRS(PE) significantly more than did cardiac beta-adrenergic receptor blockade with propranolol (72+/-4.6 vs. 43+/-2.7; p < 0.01), which suggests greater dependence of BRS(PE) on the parasympathetic component. In females, muscarinic and beta-adrenergic blockade elicited similar attenuation of BRS(PE). The findings suggest that (i) BRS is differentially influenced by gender; female rats exhibit substantially lower BRS(PE) but similar BRS(NP) compared with age-matched male rats and (ii) the sexual dimorphism in BRS(PE) results, at least partly, from a smaller increase in vagal outflow to the heart in response to baroreceptor activation.

Adrenergic beta-Antagonists↗

PubMed2001

Rapid recovery of spontaneous baroreflex after sevoflurane anesthesia in ambulatory surgery.

BACKGROUND: Although sevoflurane seems to have fulfilled the criteria of ideal anesthetic agent for ambulatory surgery, its effects on intraoperative alteration and postoperative recovery of arterial baroreflex have not been well documented. This study assessed the time required for patients anesthetized with sevoflurane to regain their baseline baroreflex after ambulatory surgeries. METHODS: Ten ASA class I female patients scheduled for minor gynecological operation (D&C) were enrolled in this study. Spontaneous baroreflex sensitivity (SBR) calculated by sequence analysis of beat-to-beat variations in systolic arterial pressure and R-R intervals was recorded before anesthesia (Baseline), during anesthesia (Anesthesia), five min after operation (Post-op 1) and ten min after operation (Post-op 2). Data obtained from Anesthesia, Post-op 1, and Post-op 2 was compared with the Baseline. RESULTS: SBR value determined in Baseline group (28.6 +/- 4.9 ms/mmHg) was significantly different from Anesthesia group (12.2 +/- 2.1 ms/mmHg) and Post-op 1 group (15.8 +/- 1.8 ms/mmHg). Patients regained their conscious baseline baroreflex sensitivity within ten min after sevoflurane was switched off. CONCLUSIONS: Sevoflurane anesthesia depresses SBR and provides a quick SBR recovery upon emergence.

Adult↗

PubMed1992

Baroreflex changes produced by serotonergic or catecholaminergic lesions in the rat nucleus tractus solitarius.

To distinguish between catecholaminergic and serotonergic mechanisms for baroreflex regulation in the medulla, we compared rats with chemical lesions produced by injecting 6-hydroxydopamine (6-OHDA) or 5,7-dihydroxytryptamine (5,7-DHT) into the nucleus tractus solitarius (NTS) bilaterally at the caudal tip of the area postrema. After 2 weeks, basal blood pressure and heart rate were unaltered, but blood pressure lability, instead of being increased, was slightly reduced. Baroreflex tests in conscious rats showed that although phenylephrine-induced reflex bradycardia was unaffected, nitroprusside-induced reflex tachycardia was enhanced by 5,7-DHT. In anesthetized rats, drug-induced reflex chronotropic responses no longer differed between groups, but attendant decreases or increases in renal nerve activity were consistently reduced by 6-OHDA. On the other hand, upon afferent aortic nerve stimulation, particularly with low current frequencies, bradycardic and sympathoinhibitory responses were enhanced by 5,7-DHT, but the sympathoinhibitory responses were reduced by 6-OHDA. Despite the absence of demonstrable necrosis or cell loss at NTS injection sites, 6-OHDA reduced norepinephrine mainly and serotonin partly, whereas 5-7-DHT reduced serotonin content alone, thereby indicating that chemical lesions had indeed been produced. Because these cardiovascular changes probably reflect differences in catecholaminergic vs. serotonergic baroreflex regulation, our results are generally compatible with the interpretation that baroreflex modulation in the NTS involves catecholaminergic facilitation and serotonergic inhibition.

5,7-Dihydroxytryptamine↗

PubMed1991

[The facilitating effect of atrial natriuretic factor on the carotid sinus baroreflex function].

Effects of atriopeptin II (APII) on the carotid sinus baroreflex in anesthetized rats and on the sinus nerve afferent activity in the anesthetized rabbits were investigated. The results were as follows: (1) By perfusing the isolated left carotid sinus with APII (1 microgram/ml) in anesthetized rats (n = 10), the threshold pressure (TP) of the carotid baroreflex did not show any change, while the equilibrium pressure (EP), the saturation pressure (SP) and the operating range (OR) were decreased from 101 +/- 2.8 to 95 +/- 2.0 mmHg (P less than 0.05), 202 +/- 5.2 to 168 +/- 6.1 mmHg (P less than 0.001) and 128 +/- 5.5 to 93 +/- 6.3 mmHg (P less than 0.001), respectively. The function curve of the baroreflex was shifted to the left and downward with a peak slope (PS) increased during perfusing with APII. In contrast, by perfusing the carotid sinus with sodium nitroprusside (NP, 0.5 micrograms/ml), TP and EP remained unchanged, whereas SP and OR were increased from 188 +/- 6.4 to 218 +/- 6.0 mmHg (n = 6, P less than 0.01) and from 107 +/- 6.9 to 132 +/- 7.6 mmHg (P less than 0.05), respectively. The function curve of the baroreflex and its PS were not affected by NP. The sinus nerve afferent activity was quite stable with the perfusion of carotid sinus at constant intrasinus pressure (ISP) in the rabbits (n = 6) and increased during the elevation of ISP.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗

PubMed1991

A statistical note on the redundancy of nine standard baroreflex parameters.

An accepted method for measuring the responsiveness of the carotid-cardiac baroreflex to arterial pressure changes is to artificially stimulate the baroreceptors in the neck with a pressurized neck chamber. Nine physiological responses to this type of stimulation are quantified and used as indicators of the baroreflex response function. Thirty male humans between the ages of 27 and 46 underwent the carotid-cardiac baroreflex test. The data for the nine response parameters were analyzed by principle component factor analysis. The results indicated that 92.5% of the total variance across all nine parameters could be explained in four dimensions. The first two dimensions reflected location points for R-R interval and carotid distending pressure, respectively. The third factor was composed of measures reflecting the gain (responsiveness) of the reflex. The fourth dimension was the ratio of baseline R-R interval to the maximal R-R interval response during simulated hypertension. The data suggest that the analysis of all nine baroreflex parameters is likely to be redundant and researchers should account for these redundancies either in their analyses or conclusions.

Adult↗

PubMed1990

Influence of general anesthetics on baroreflex control of circulation.

1. The effects of sodium pentobarbital and alpha-chloralose anesthesia on the baroreflex control of circulation were studied in groups of 7 to 11 rats. The tests were performed in conscious undisturbed rats and repeated after anesthesia. 2. Pentobarbital (15 min) depressed the initial peak of the pressor response produced by carotid occlusion by 68% (15 +/- 1 vs 47 +/- 3 mmHg) and the maintained response by 52% (13 +/- 1 vs 27 +/- 4). Depression by chloralose was 48% (26 +/- 5 vs 50 +/- 3) and 21% (19 +/- 2 vs 24 +/- 3), respectively. The inhibition progressively declined at 30, 60, 90 and 120 min after pentobarbital but was unchanged up to 120 min after chloralose. 3. The baroreflex sensitivity index for bradycardic responses (phenylephrine injection) diminished by 50% after pentobarbital (-1.1 +/- 0.3 vs -2.2 +/- 0.3 beats/min per mmHg) and remained unaltered after chloralose. 4. The baroreflex sensitivity index for tachycardic responses (nitroprusside injection) was depressed by 61% after pentobarbital (-1.5 +/- 0.5 vs -3.8 +/- 0.5 beats/min per mmHg) and 35% after chloralose (-2.5 +/- 0.2 vs -3.9 +/- 0.5). 5. In general the depression of reflex control of circulation was more severe after pentobarbital than after chloralose anesthesia, while the resting control arterial pressure was not affected by either. The inhibition of the baroreflex tachycardic responses was more intense than that of the bradycardic responses and represented a better index of the depression exerted on the pressure responses to carotid occlusion.

Animals↗

PubMed1990

Age-dependent baroreflex attenuation by centrally infused verapamil in rats.

Because oral administration of verapamil for 6 days reduces reflex tachycardia without affecting reflex bradycardia, we tested chronotropic baroreflexes in conscious rats aged 5 or 15 months before and after verapamil was infused intracerebroventricularly for 6 days to determine whether a central action contributes to the reflex attenuation. Baroreflex responses consisted of reflex bradycardia elicited during pressor responses to methoxamine and reflex tachycardia during depressor responses to sodium nitroprusside. As we have shown previously, all reflex heart rate responses were initially smaller in 15-month-old than in 5-month old rats. Osmotic minipumps filled with saline or verapamil (100 micrograms/kg/day) were connected to cannulas in a lateral ventricle or femoral vein and, after 6 days, baroreflexes were recorded again. Control infusions of either saline intracerebroventricularly or verapamil intravenously were ineffective. In contrast, intracerebroventricular infusions of verapamil attenuated reflex heart rate responses to methoxamine or sodium nitroprusside differently in the two age groups: both reflex tachycardia and bradycardia were attenuated in 5-month-old rats; however, in 15-month-old rats only reflex bradycardia was reduced, whereas reflex tachycardia was unaffected. The selective reduction of reflex tachycardia in 5-month-old, but not in 15-month-old, rats suggests that intracerebroventricularly infused verapamil affects central baroreflex regulation differently depending on age.

Age Factors↗

PubMed1985

The role of baroreflex sensitivity in post-exercise hypotension.

We investigated whether changes in baroreflex sensitivity could explain the drop in blood pressure after exercise in 12 borderline hypertensive subjects. Intra-arterial blood pressure and baroreflex sensitivity (phenylephrine method) were measured before and 10, 20, 40 and 60 min after maximal exercise. Systolic blood pressure was lower at all stages after exercise. Baroreflex sensitivity was reduced at 10 min, recovered at 20 min and rose above control values at 40 and 60 min. Although the baroreflex sensitivity recovers slowly after exercise, at 40 and 60 min it is higher than the control value and could therefore contribute to the sustained reduction in blood pressure after a period of heavy exercise.

Blood Pressure↗

PubMed1987

Difference between intracarotid and intravenous infusions of angiotensin II on baroreflex sensitivity and vasopressin release in conscious rats.

A carotid infusion of angiotensin (AII) (10 ng/kg/min) has been found to increase significantly higher mean arterial pressure (MAP) and produces significantly lower bradycardia than AII intravenous infusions at the same dose and rate. Besides, i.v. administration of AII elicits greater impairment on baroreflex sensitivity than carotid infusion of AII does. On the other hand, vasopressin vascular receptor blockade did not modify the baroreflex sensitivity either in the carotid or in the i.v. infusions of AII, and plasma AVP measurements did not change significantly in any group. It clearly indicates that neither AVP nor baroreflex impairment plays any role on the pressor action of AII intracarotid infusions at a low dose. The present results further suggest that baroreflex impairment in rats may unlikely be located in the region irrigated by the carotid artery.

Angiotensin II↗

PubMed1987

Effect of propofol anesthesia on baroreflex activity in humans.

Previous studies have shown that infusions of propofol, a new intravenous anesthetic, were associated with decreased arterial pressure and slow heart rates. To evaluate the role of baroreflex mechanisms in sustaining these conditions, the effects of two infusion rates of propofol (54 and 108 micrograms.kg-1.min-1) to supplement 66% nitrous oxide in oxygen anesthesia were studied in twelve ASA class I patients having a mean age of 34 years. Baroreflex control of heart rate was studied by perturbing the patients' arterial pressure with phenylephrine or sodium nitroprusside. Valsalva maneuvers were used to assess the response of the systemic arterial system. Steady state anesthesia at both infusion rates was not associated with decreased sensitivity of the baroreflex control of heart rate, but resetting of the reflex occurred to allow lower arterial pressures for a given heart rate than in the awake state. During propofol infusions at either rate, the diastolic pressure overshoot normally associated with the relief of raised airway pressure in the Valsalva maneuver was significantly reduced. It is concluded that propofol/nitrous oxide anesthesia is not associated with impairment of baroreflex sensitivity, but that central sympatholytic and/or vagotonic mechanisms enable low heart rates to be sustained despite decreased arterial pressures.

Adult↗

PubMed1987

Control of lumbar sympathetic nerve traffic by vagal cardiopulmonary baroreflexes in renal hypertension.

Renal nerve traffic is inhibited during volume expansion mainly because of stimulation of vagal cardiopulmonary baroreflexes. These responses are impaired in rabbits with renal hypertension caused by impaired cardiopulmonary baroreflexes. Previous studies have suggested that there may be differences in the extent to which renal hypertension alters reflex control of lumbar as compared with renal sympathetic nerve activity. The goals of this study were to determine if the responses to volume expansion of lumbar sympathetic nerve traffic also are impaired in renal hypertension and if this abnormality, if present, is caused by abnormalities in the vagal cardiopulmonary baroreflex. Experiments were done in alpha-chloralose-anesthetized normotensive (n = 9) and renal hypertensive (n = 7; 1 kidney, 1 wrap) rabbits. Infusion of dextran in saline raised arterial and left atrial pressures in both groups and decreased lumbar nerve traffic by -4.4 +/- 0.4% mm Hg rise in arterial pressure in the normotensive group and by -1.5 +/- 0.1% mm Hg in the hypertensive group (p less than 0.01). These responses were nearly abolished by sinoaortic denervation in both groups. These data indicate that the responses of lumbar nerve traffic to volume expansion are impaired in renal hypertension; this is mainly because of impaired arterial baroreflexes since vagal cardiopulmonary baroreceptors have minimal influence on lumbar nerve traffic, even in normotensive rabbits. These findings for the lumbar nerves are strikingly different from those reported previously for reflex control of the renal nerves in both normotensive and hypertensive rabbits.

Animals↗

PubMed1987

Baroreflex control of renal nerve activity in conscious animals.

This study quantitates the effect of three different doses of vasopressin on the arterial baroreflex control of renal sympathetic nerve activity and heart rate. The lowest dose of vasopressin (0.4 mU/kg X min), which had no significant effect on resting mean arterial pressure, heart rate, or renal sympathetic nerve activity, increased the inhibitory influence of arterial baroreflexes on renal sympathetic nerve activity in response to an increase in pressure. During infusions of higher doses of vasopressin (1.5 and 3.0 mU/kg X min), which significantly decreased resting heart rate and renal sympathetic nerve activity but had no significant effect on mean arterial pressure, the mean arterial pressure-renal sympathetic nerve activity relation showed a significant decrease in maximum renal sympathetic nerve activity when compared with control. The highest dose of vasopressin resulted in a significant shift of the relation to the left toward lower pressures and in a decrease in maximum gain. The relation exhibited a parallel shift toward lower pressure, with no change in gain, at the higher dose of vasopressin. Based on these results, we conclude that vasopressin exerted a dose-related effect on arterial baroreflex such that lower doses of vasopressin may sensitize the central baroreflex neurons to afferent input, while the higher doses of vasopressin caused direct excitations of these neurons, resulting in a reduction in resting sympathetic outflow.

Animals↗

PubMed1984

Abnormal baroreflex control of heart rate in normotensive young subjects with a family history of essential hypertension.

This study was performed to determine whether baroreflex control of heart rate is impaired in young normotensive subjects with hypertensive relatives. Blood pressure, baroreflex function, pressor response to phenylephrine, aortic distensibility (pulse pressure/stroke volume) and minimal forearm vascular resistance (minFVR) were assessed in 13 normotensive subjects with hypertensive relatives (group A) and 11 normotensive subjects with no family history of hypertension (group B). Baroreflex sensitivity was significantly lower in group A than in group B (9.4 +/- 1.7 versus 17.5 +/- 1.7 ms/mmHg, P less than 0.01), although blood pressure, aortic distensibility and minFVR were not different between two groups. Pressor response to phenylephrine was identical for both groups. These results suggest that baroreflex control of heart rate is impaired in normotensive young subjects with hypertensive relatives and this defect may be inherited rather than the result of elevated blood pressure and decrease aortic distensibility.

Adult↗

PubMed1983

Baroreflex control of heart rate during cardiac sympathectomy by epidural anesthesia in lightly anesthetized humans.

To evaluate the effects of acute sympathetic denervation on the baroreflex control of heart rate, baroreflex sensitivities were compared in lightly anesthetized humans who had either cervical (N = 20) or lumbar epidural anesthesia (N = 18), or neither (N = 18). Levels of anesthesia during cervical block using 10 ml of 2% mepivacaine without epinephrine were C3-T7 and T7-S1 during lumbar epidural block. Baroreflex sensitivity was assessed with a pressor test using phenylephrine infusion to increase systolic blood pressure by 60 mm Hg within 2 min. There were no statistically significant differences in the baroreflex sensitivities in the absence of epidural block and during lumbar epidural block, the slopes of the regression line (in msec of RR interval change per mm Hg increase in systolic blood pressure, i.e., msec/mm Hg) relating systolic pressure and the succeeding pulse interval being 3.8 +/- 1.4 (mean +/- SD) and 3.7 +/- 1.7, respectively. The mean slope during cervical block, 1.1 +/- 1.2 msec/mm Hg, was significantly different from the slopes observed in the absence of epidural block and during lumbar epidural block (P less than 0.01). The results suggest that cardiac sympathectomy induced by epidural anesthesia can suppress partially baroreceptor function by interrupting sympathetic efferent fibers innervating the heart during high levels of epidural anesthesia, but that lumbar sympathectomy during epidural anesthesia is unlikely to affect baroreceptor activity.

Adult↗