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PubMed1989

Antihypertensive drugs and baroreflex sensitivity. Effects of rilmenidine.

Rilmenidine 1 and 2 mg administered orally (weekly intervals, double-blind, randomized cross-over, placebo-controlled) to six healthy subjects, dose-dependently reduced (p less than 0.05) resting systolic blood pressure (107.0 +/- 5.6, 99.2 +/- 4.5 mmHg) compared with placebo (117.3 +/- 5.2 mmHg). Diastolic blood pressure was also reduced (p less than 0.05), and no change occurred in heart rate or forearm blood flow. Rilmenidine increased (p = 0.05) baroreflex sensitivity when blood pressure was increased with phenylephrine: no change in baroreflex sensitivity occurred during reduction in blood pressure with glyceryl trinitrate. Rilmenidine given at 1- and 2-mg doses reduced (p less than 0.05) systolic blood pressure during "lying to standing," a test of autonomic function (76.3 +/- 9.8, 56.8 +/- 4.5 mmHg), versus results with placebo (95.2 +/- 10.5 mmHg); the R-R intervals associated with these blood pressure reductions were not different (571 +/- 12, 609 +/- 19 msec), versus results with placebo (541 +/- 28 msec). During "sustained handgrip," rilmenidine given at 1- and 2-mg doses reduced (p less than 0.05) systolic blood pressure (146.8 +/- 6.2, 142.3 +/- 7.0 mmHg), versus results with placebo (157.3 +/- 7.5 mmHg); the corresponding R-R intervals were 705 +/- 45 and 675 +/- 49 msec, not different from those with placebo (695 +/- 49 msec). Similar results occurred with other tests of autonomic function ("deep breathing" and "three-minute standing"). In conclusion, rilmenidine increases baroreflex sensitivity to increases in blood pressure with phenylephrine; during tests of autonomic function, the lower blood pressures that occur with rilmenidine are associated with correspondingly greater R-R intervals; this may also indicate enhanced baroreflex sensitivity.

Adult↗
PubMed1992

Importance of cardiac, but not vascular, hypertrophy in the cardiac baroreflex deficit in spontaneously hypertensive and stroke-prone rats.

In the present study, we examined whether antihypertensive treatment of young and adult hypertensive rats with the angiotensin-converting enzyme (ACE) inhibitor perindopril could restore the baroreflex vagal deficit and whether this was related to prevention of cardiac or vascular hypertrophy. Spontaneously hypertensive (SHR), stroke-prone spontaneously hypertensive (SHR-SP), and Wistar-Kyoto (WKY) rats were untreated or treated with perindopril (3 mg/kg/day) in the drinking water from 4-9 and from 14-20 weeks of age. Steady-state sigmoidal mean arterial pressure (MAP)-heart rate (HR) reflex curves were obtained in the conscious rats by the injection of pressor and depressor agents before and after atenolol (vagal component). Increased left ventricle to bodyweight ratio (LV/BW) indicated cardiac hypertrophy. After ganglion blockade, the minimum MAP produced by nitroprusside and the maximum produced by methoxamine were used as indications of vascular hypertrophy. Perindopril treatment reduced cardiac and vascular hypertrophy to different extents in SHR and SHR-SP. The 4-9 and 14-20 week treatments reduced MAP and both minimum and maximum blood pressure of the SHR to the levels of the untreated WKY. However, only in the older animals was LV/BW restored. In the SHR-SP, early treatment had a much greater effect on vascular hypertrophy than on LV/BW. The reverse occurred for the 14-20 week animals. In untreated hypertensive animals the baroreflex curves were shifted to the right with reduced vagal HR range. Perindopril treatment shifted the baroreflex curves back towards the WKY curves. Vagal HR range was strongly correlated with the LV/BW, whereas vagal HR range was less well related to the level of vascular hypertrophy or blood pressure. These results suggest that antihypertensive treatment can restore cardiac baroreflex function and that it is related to the reduction in cardiac hypertrophy. Although the mechanism of this relationship remains to be elucidated, these findings suggest that cardiac vagal afferents may be important.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

Facilitation of baroreflex-induced bradycardia by stimulation of specific hypothalamic sites in the rat.

Hypothalamic stimulation generally inhibits baroreflex-induced bradycardia. However, we have noted discrete areas of the rat hypothalamus which facilitate reflex bradycardia. The effects of hypothalamic stimulation on baroreflex-induced changes in heart rate were investigated in urethane-anesthetized rats (1.2 g/kg, i.p.; n = 6) instrumented with femoral arterial and venous catheters. Bipolar electrodes (250 micron diameter) were implanted stereotaxically in the hypothalamus. Baroreflex-induced bradycardia was elicited by phenylephrine (PE) injection (8-20 micrograms/kg). Responses to stimulation (STIM) (50-150 microA, 80 Hz, 0.5 ms), PE, and Stim + PE were studied for 1 min. In the ventral medial and anterior hypothalamus, STIM caused transient increases in blood pressure and no changes in heart rate. Peak blood pressure was lower during STIM + PE than during PE (144 +/- 5 vs 164 +/- 3 mm Hg; P less than 0.05). However, STIM + PE resulted in a lower heart rate compared to PE (194 +/- 22 22 vs 270 +/- 17 bpm; P less than 0.05). At 1 min, the heart rate in STIM + PE rats remained lower than in PE rats (205 +/- 37 vs 319 +/- 16 bpm; P less than 0.05). Atropine administration indicated that the facilitation was primarily parasympathetic in nature. These results identify specific hypothalamic regions which facilitate baroreflex-induced bradycardia by parasympathetic mechanisms.

Animals↗
PubMed1987

Role of excitatory amino acids in rat vagal and sympathetic baroreflexes.

Vagal baroreflexes were studied by measuring the atropine-sensitive cardioinhibition produced by raising arterial pressure with phenylephrine in anesthetized rats pretreated with the beta-adrenergic receptor antagonist nadolol. Sympathetic baroreflexes were determined in halothane-anesthetized rats by measuring the inhibition of lumbar sympathetic discharge produced by elevating arterial pressure with gradual aortic constriction. Both reflexes were drastically reduced by bilateral injections of 2.2 nmol of the glutamate receptor antagonist kynurenic acid (KYN) into either the nucleus of the solitary tract (NTS) or the ventrolateral medulla between 0 and 1 mm posterior to the level of the obex. Injections of KYN elsewhere in the medulla were generally ineffective and injections of 8-OH kynurenate (an inactive analog) into the ventrolateral medulla or NTS were also without effect. KYN injections (2.2 nmol) into the intermediate portion of the NTS produced small increases in mean arterial pressure (0-15 mm Hg) and no change in heart rate while injections of similar amounts into the ventrolateral medulla at obex level were followed by large (35-116 mm Hg) increases in pressure and bradycardia. Both types of injections produced a similar degree of blockade of vagal and sympathetic baroreflexes. These results support previous evidence that baroreceptor primary afferents may release a glutamate-like transmitter in the NTS and indicate that a similar type of excitatory transmitter is involved at the level of the ventrolateral medulla in mediating or modulating both vagal and sympathetic baroreflexes. Finally the bradycardia and hypertension produced by blocking amino acid receptors in the ventrolateral medulla appear largely unrelated to the disruption of peripheral baroreceptor inputs.

Amino Acids↗
PubMed1978

Effect of d,l-propranolol on renal sympathetic baroreflex properties and aortic baroreceptor activity.

Sigmoid renal baroreflex curves relating mean arterial pressure to integrated renal sympathetic nerve activity were obtained in anaesthetized rabbits with previously implanted balloons to raise and lower blood pressure. Propranolol was infused to reach plasma levels averaging 324 ng/ml. This reduced blood pressure by 9.6 +/- 1.1 mm Hg, but had no effect on resting sympathetic discharge. Propranolol lowered the threshold of the renal baroreflex. Median blood pressure was reduced by 15.4 +/- 1.9 mmHg but there was no change in gain or sympathetic activity range. Thus, at a given blood pressure there was diminution of sympathetic discharge compared with control. Similar changes occurred after giving clonidine. However, "non-specific" produced by bleeding or nitroprusside infusion produced no resetting of the baroreflex curves, though the resting sympathetic discharge increased. The effects of propranolol (plasma levels 137 and 348 ng/ml) on arterial baroreceptor discharge were studied by deriving mean arterial pressure-integrated aortic nerve activity curves. Propranolol produced a reduction of aortic nerve discharge of about 7% of control. Single unit analysis showed a small reduction in firing frequency/sec near threshold, which was sufficient to explain the changes in integrated aortic nerve discharge. Since the changes in input from the aortic baroreceptors do not account for the reduction in threshold of the renal baroreflex, we conclude that the latter is due to the central nervous action of propranolol.

Animals↗
PubMed1983

Effect of naloxone on baroreflex, sympathetic tone and blood pressure in the cat.

Studies were designed to determine the effect of naloxone on sympathetic nerve activity and blood pressure and, also to investigate the central effect of naloxone in relation to the baroreflex system in alpha-chloralose-anesthetized cats. Following intravenous injection of naloxone (2 mg/kg), preganglionic splanchnic nerve (PSN) activity significantly increased in parallel to the increase in blood pressure. Set gain (mmHg-1) of carotid sinus baroreflex together with the operational range (mmHg) was increased after naloxone. Intraventricular (4th) injection of naloxone (0.2 mg/kg) produced identical responses in blood pressure and PSN activity as well as an altered set gain and range of the baroreflex. Additionally, the pressor response to carotid hypotension and medullary pressor area stimulation were augmented during naloxone activation but not the pressor response to posterior hypothalamus stimulation. The depressor responses to stimulation of both carotid sinus nerve and medullary depressor region were facilitated by naloxone. These data suggest that naloxone has an effect on the central autonomic blood pressure regulatory circuits which participate in the carotid sinus baroreflex system.

Animals↗
PubMed1990

Acute and chronic effects of rilmenidine on baroreflex function in conscious dogs.

The effects of acute and chronic administration of rilmenidine on blood pressure, heart rate and baroreflex function were assessed in two groups of six conscious dogs. Baroreflex function was evaluated using increasing doses of glyceryl trinitrate and phenylephrine to decrease and increase blood pressure respectfully. Acute administration of rilmenidine (1 mg/kg p.o.) reduced (P less than 0.05) blood pressure and heart rate, and enhanced (P less than 0.05) baroreflex function to increases in blood pressure with phenylephrine, but not to decreases in blood pressure by glyceryl trinitrate. Following chronic administration of rilmenidine, blood pressure remained lowered while heart rate and baroreflex function returned to control values.

Adrenergic alpha-Agonists↗
PubMed1991

Baroreflex sensitivity at rest and during stress in individuals with a history of vasovagal syncope.

The baroreflex sensitivity of healthy young adult males who reported some history of vasovagal syncope during emotionally stressful situations (e.g. blood donation) was compared to a control group of individuals who reported no such history. The baroreflex, which induces compensatory bradycardia and vasodilation in response to acute elevations of blood pressure, was examined as a possible mechanism underlying predisposition to vasovagal reactions. Changes in heart rate and vasoconstriction in response to baroreflex stimulation (negative external cervical pressure) at rest and during administration of a mental arithmetic task and a constrictive pain stimulus were assessed. Individuals with a history of vasovagal reactions displayed greater baroreflex sensitivity during the pain stimulus and at rest, but not during mental arithmetic. These findings suggest one mechanism of risk for syncope reactions, particularly in situations involving the experience of pain.

Adult↗
PubMed1992

Catecholaminergic nucleus tractus solitarius lesions in anesthetized rats alter baroreflexes differently with age.

To explore whether catecholaminergic lesions produced chemically in the nucleus tractus solitarius (NTS) would alter the baroreflex impairment that normally occurs with age, we compared baroreflex responses in 3- and 14-month-old rats given bilateral microinjections of 6-hydroxydopamine (6-OHDA) or its vehicle into the NTS. After 2 weeks, basal pressures were unaffected but heart rates were lower in 14- than in 3-month-old rats. Sympathetic nerve inhibition elicited reflexly during intravenous infusions of sodium nitroprusside was reduced in 3-month-old rats, but increased in 14-month-old rats. Depressor, bradycardiac, and sympatho-inhibitory responses to afferent aortic nerve stimulation were likewise reduced in 3-month-old rats and oppositely enhanced in 14-month-old rats. Enhanced bradycardia probably does not depend on increased parasympathetic sensitivity because responses to vagal stimulation did not differ between age groups. Although underlying mechanisms remain uncertain, by showing that baroreflex responses become altered differently in 3- and 14-month-old rats by 6-OHDA these results suggest that the baroreflex changes normally occurring with age may be due, at least in part, to modified catecholaminergic mechanisms in the NTS.

Aging↗
PubMedDate not supplied

Central nervous system opiate and 5-hydroxytryptamine influences on baroreflex control of the coronary circulation.

The effect of intravenous infusion of fentanyl (an opiate receptor agonist, 0.55 microgram kg-1 min-1) on the control of the circumflex coronary circulation was examined in unsedated dogs at rest and during baroreceptor stimulation evoked by acute rises in aortic pressure (balloon inflation in thoracic aorta). Circumflex flow was measured using Doppler flow transducers in dogs with experimental complete heart block and with ventricles paced at a constant rate. Studies were also performed before and one week after intracisternal injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT), to examine the role of CNS 5-hydroxytryptamine (5-HT) in any sympathetic vasoconstrictive effects. Fentanyl infusion caused after a few minutes a progressive rise in resting aortic pressure and a significant fall in circumflex conductance; circumflex flow usually fell. Atrial rate also fell. The gain of the baroreflex control of circumflex conductance was enhanced by fentanyl. One week after intracisternal 5,7-DHT, the gain of the baroreflex in each dog was diminished. When fentanyl was infused into these preparations, no consistent changes in resting atrial rate, aortic pressure and circumflex conductance could be observed, but all dogs showed a recovery of the coronary baroreflex gain towards values observed before intracisternal 5,7-DHT. These data suggest that the gain control of coronary baroreflexes is influenced by CNS opiate and 5-HT dependent mechanisms.

5,7-Dihydroxytryptamine↗
PubMed1989

Kynurenic acid microinjected into the nucleus tractus solitarius of rat blocks the arterial baroreflex but not responses to glutamate.

The selective excitatory amino acid antagonist kynurenic acid was bilaterally microinjected into the nucleus tractus solitarius of rats to determine its effects on the arterial baroreflex and on the cardiovascular responses to glutamate and nonglutamate agonists injected at the same site. Kynurenic acid blocked the responses to N-methyl-D-aspartate and kainate as well as the baroreflex, but did not block the response to glutamate, quisqualate, or acetylcholine. The data may suggest that glutamate is not a neurotransmitter in the baroreflex arc or that only certain glutamate receptors are integral to the baroreflex in the nucleus tractus solitarius.

Acetylcholine↗
PubMed2000

Altered baroreflex responses in alpha7 deficient mice.

The autonomic nervous system controls and coordinates several cardiovascular functions, including heart rate, arterial pressure, blood flow and vasomotor tone. Neuronal nicotinic acetylcholine receptors (nAChRs) are the interface between the nervous system and the cardiovascular system, but it is not known which nAChR subtypes regulate autonomic function in vivo. Nicotinic AChRs containing the alpha7 subunit are a candidate subtype in autonomic ganglia. Stimulation of these nAChRs can increase neurotransmitter release via presynaptic mechanisms, as well as mediate fast synaptic transmission via postsynaptic mechanisms. To investigate the role of the alpha7 nAChR subunit in cardiac autonomic function, we measured baroreflex-mediated responses in alpha7 null mice. Here we show that the alpha7 null mice have impaired sympathetic responses to vasodilatation, as sodium nitroprusside infusion triggered a 48% heart rate increase in wild type mice but only a 21% increase in the alpha7 nulls (P < 0.001). The mutant mice developed supersensitivity to adrenergic agonists, although norepinephrine release from sympathetic nerve terminals could be elicited through mechanisms alternative to nAChR stimulation. Baroreflex-mediated parasympathetic responses were normal in alpha7 null mice. The decreased baroreflex-mediated tachycardia in alpha7 mutant mice indicates that alpha7-containing nAChRs participate in the autonomic reflex that maintains blood pressure homeostasis. The alpha7 mutant mice may serve as a model of baroreflex impairment arising from autonomic dysfunction.

Animals↗
PubMed1995

Learning of physiological responses: II. Classical conditioning of the baroreflex.

The baroreflex can be classically conditioned. In neuromuscular blocked (NMB) rats, electrical stimulation of the aortic depressor nerve (ADN) and dopamine-produced blood pressure rise were effective unconditioned stimuli (UCS) for auditory discriminative classical conditioning. The conditioned response (CR) pattern (bradycardia, vasodilatation, and hypotension > 10 torr) closely resembled that of the unconditioned baroreflex. Conditioned stimulus (CS) specificity was demonstrated by discrimination of baroreflex-associated and nonassociated auditory stimuli, and also by elaborating depressor and pressor CRs to auditory CSs, which respectively had been associated with either baro-afferent (depressor) or tail-shock (pressor) UCSs. The conditioned-baroreflex-magnitude increased with trials. These findings support quantitative models in which CRs interact with and calibrate the gain and dynamic properties of natural reflexes.

Acoustic Stimulation↗
PubMed1990

Effects of caffeine on baroreflex activity in humans.

The effects of caffeine or placebo on blood pressure, heart rate, and baroreflex activation (elicited by phenylephrine) were studied on young normotensive volunteers after a 7-day caffeine-free period. Subjects received oral doses of either 250 mg caffeine (n = 6) or placebo (n = 4), and hemodynamic changes were studied at 0, 30, 60, 120, and 180 minutes after drug administration. Thirty minutes after the caffeine dose, blood pressure had risen from 127 +/- 8/57 +/- 4 mm Hg to 136 +/- 3/68 +/- 5 mm Hg, heart rate was unchanged, and the baroreflex slope had decreased from 31 +/- 7 msec/mm Hg to 11.6 +/- 2 msec/mm Hg. Baroreflex sensitivity remained inhibited for the rest of the single-dose experimental period. In contrast, no significant changes were observed after either long-term caffeine ingestion in the same group or in the placebo group during the single- or multiple-dose study. These findings indicate that single but not multiple caffeine administration inhibits baroreflex activation in normotensive volunteers and this could contribute to the acute hemodynamic effects of caffeine.

Administration, Oral↗
PubMed1978

The effect of mental arithmetic on blood pressure variability and baroreflex sensitivity in man.

1. Baroreflex sensitivity was tested in three normal, three borderline and one hypertensive subject before and during mental arithmetic, the prolongation of pulse interval caused by a provoked rise in blood pressure being used as a measure of baroreflex sensitivity. 2. Baroreflex sensitivity was significantly decreased during mental arithmetic. 3. During mental arithmetic the arterial pressure fluctuated markedly. 4. These findings suggest that in man, as well as animals, the defence of alerting reaction depresses baroreflex control and thus contributes to the rise in blood pressure seen at this time.

Blood Pressure↗
PubMed1982

Baroreflex sensitivity during the development of spontaneous hypertension in rats.

1. Baroreflex sensitivity was studied in relation to the development of spontaneous hypertension in rats (SH rats), with normotensive Wistar-Kyoto (WKY) rats as controls. Conscious, freely moving animals were studied at different times, ranging from 4 to 20 weeks after birth. 2. The youngest SH rats (4-6 weeks; n = 10) already had significantly (P less than 0.01) higher mean arterial blood pressure (112 +/- 2 mmHg) than WKY rats of corresponding age (95 +/- 4 mmHg; n = 10). Baroreflex sensitivity did not differ at this age (0.37 +/- 0.04 vs 0.38 +/- 0.05 ms/mmHg). 3. Mean arterial pressure increased rapidly in SH rats during further development, reaching a value of 166 +/- 3 mmHg in 12-20 week old animals (n = 25). In equally old WKY rats blood pressure was significantly (P less than 0.001) lower (110 +/- 6 mmHg, n = 25). Baroreflex sensitivity did not change during development of SH rats (0.40 +/- 0.03 ms/mmHg in 12-20 weeks old SH rats), whereas it increased two- to three-fold in WKY rats (0.93 +/- 0.08 ms/mmHg, P less than 0.001). 4. It is concluded that an increase in baroreflex sensitivity is part of the development of a normotensive cardiovascular system, whereas in SH rats responsiveness of the baroreceptor reflex remains depressed during the development and stabilization of hypertension.

Animals↗
PubMed1985

Exercise blood pressure and baroreflex function in borderline hypertensive and normotensive young men.

1. Resting carotid baroreflex sensitivity and blood pressure responses to standardized conditions of rest and exercise were measured in 17 borderline hypertensive males and 12 normotensive males. 2. The borderline hypertensive group had significantly higher systolic and diastolic blood pressures during orthostatic rest and isometric handgrip exercise and higher systolic blood pressure during supine rest and submaximum and maximum treadmill exercise. 3. The borderline hypertensive group had an attenuation of baroreflex sensitivity compared with the normotensive group. Resting baroreflex sensitivity was significantly correlated with absolute systolic blood pressure during supine rest, orthostatic rest, isometric handgrip exercise and submaximum treadmill exercise. 4. The results indicate that blood pressure is regulated at a significantly higher level during rest and exercise in borderline hypertension and is associated with reduced baroreflex sensitivity measured at supine rest.

Adult↗
PubMed1988

Central attenuation of baroreflex by angiotensin II in normotensive and spontaneously hypertensive rats.

To determine whether angiotensin II (A II) can modify baroreflex centrally and contribute to the central resetting of baroreflex in spontaneously hypertensive rats (SHRs), the aortic depressor nerve (ADN) was electrically stimulated following intracerebroventricular (ICV) administration of A II and/or A II analog in urethane-anesthetized normotensive Wistar rats (WKYs) and SHRs. Electric stimulation of the ADN elicited frequency-dependent depressor, bradycardic, and sympatho-inhibitory responses. Angiotensin II, administered ICV, dose-dependently attenuated these responses induced by ADN stimulation in normotensive rats. We found, however, these attenuations could be abolished by ICV pretreatment with A II analog. Vasopressin (ICV) did not change any responses to ADN stimulation. The vasopressor and sympatho-inhibitory responses to ADN stimulation were significantly less in SHRs when compared with those in WKYs: In SHRs, A II analog completely cancelled the A II-attenuated responses to ADN stimulation. These findings suggest that A II can centrally attenuate baroreflex, which might be independent from vasopressin, and in the brain A II can contribute to the central resetting of baroreflex in SHRs.

Angiotensin II↗