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PubMed2006

Impaired baroreflex sensitivity and responses to angiotensin converting enzyme inhibitor in salt-induced hypertension and its prevention by dietary calcium supplement in Sprague-Dawley rats.

The role of renin-angiotensin system and baroreceptors in the pathogenesis and prevention of hypertension due to salt-loading and concurrent dietary calcium for 6 weeks in Sprague-Dawley rats were studied. Blood pressure measurements were done in anaesthetized animals while the activities of renin-angiotensin and parasympathetic nervous systems were determined by the effect of their inhibition on the arterial pressure and baroreflex sensitivity, via captopril infusion and vagotomy respectively. The sympathetic nervous system activity and its effect on baroreflex response were estimated by combined captopril infusion and vagotomy. There was elevation of mean arterial pressure (MAP) in salt-loaded rats (SR) relative to controls (NR) (140.5 +/- 2.18 vs 98.0 +/- 1.38 mmHg) without any significant effect on heart rate (HR) (406 +/- 8.58 vs 428 +/- 11.20 beats/min). Calcium supplement abolished the rise in MAP of salt-loaded-calcium-fed rats (SCaR) (102.8 +/- 2.30 mmHg) but led to reduction in their HR (389 +/- 10.21 beats/ min) relative to control. Renin-angiotensin system inhibition led to fall in MAP in all groups of rats with the greatest reduction observed in SR. Inhibition of parasympathetic effects resulted in elevation of MAP in all thegroups. with SCaR and CaR having the highest rise. SR and SCaR had higher sympathetic activity than NR and CaR. Bilateral carotid occlusion test showed decrease baroreflex sensitivity in SR compared with NR while those of SCaR were enhanced without significantly affecting CaR. Also, there was enhanced baroreflex response (BRR) due to renin-angiotensin system inhibition in NR and SR while it was significantly reduced in SCaR but none in CaR. However, there was reduced BRR to parasympathetic inhibition in experimental groups except in CaR. Unmodified sympathetic activity resulted in enhanced BRR in all the groups. The results of the present study suggests that renin-angiotensin and autonomic nervous systems are impaired by dietary salt-loading, while prevention of salt-hypertension by calcium supplement is through modulation of these actions.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1995

[The effects of systemic bupivacaine on baroreflex sensitivity in dogs].

To evaluate the effects of systemic bupivacaine on the baroreflex control of heart rate, we investigated the baroreflex sensitivity assessed with a pressor and a depressor test using phenylephrine and nitroglycerin in pentobarbital anesthetized dogs (n = 12). Intravenous injection of bupivacaine (mean plasma concentration of 2.4 +/- 0.9 micrograms.ml-1) caused a significant suppression of the baroreflex sensitivity, defined by the slopes of regression line (in msec of RR interval change per mmHg increase or decrease in systolic blood pressure). The sensitivity obtained with the pressor and the depressor tests decreased from 6.0 +/- 2.3 to 3.5 +/- 1.7, from 2.4 +/- 1.3 to 1.3 +/- 0.8 msec.mmHg-1, respectively (P < 0.01). Suppression of the baroreflex sensitivity during epidural anesthesia with bupivacaine could be due not only to cardiac sympathectomy but also to a direct effect of bupivacaine on the reflex arch including the receptors, the afferent nerve pathways, the CNS, the efferent pathway, and the effector organs. Therefore, the hemodynamic responses to reduction of blood pressure are likely to be inhibited by epidural bupivacaine.

Anesthesia, Epidural↗
PubMed1994

Decreased cardiac baroreflex sensitivity is not due to cardiac hypertrophy in NG-nitro-L-arginine methyl ester-induced hypertension.

OBJECTIVE: To investigate the link between cardiac hypertrophy, elevated blood pressure level and baroreflex impairment, we assessed cardiac baroreflex function in a hypertensive model almost devoid of cardiac hypertrophy, obtained by nitric oxide synthesis inhibition. METHODS: Thirteen adult male Wistar rats were treated orally with NG-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg per 24 h) for 4 weeks. Fifteen control rats received tap water. At the end of the treatment aortic blood pressure was recorded continuously and the baroreceptor-heart rate curve was assessed by bolus injections of phenylephrine and sodium nitroprusside (10 different doses of each). RESULTS: Mean blood pressure was higher in L-NAME rats than in control rats, whereas body weight was similar. Total heart weight and left ventricular weight did not differ between the groups. Cardiac baroreflex was reset in hypertensive rats, as indicated by a rightwards shift of the mean blood pressure-heart rate curve. Its gain was decreased significantly in L-NAME rats, whereas the heart rate range was not different between the two groups. CONCLUSION: L-NAME hypertensive rats exhibit an original impairment of cardiac baroreflex, characterized by a range-independent decreased gain which is not due to cardiac hypertrophy.

Animals↗
PubMed1994

Postnatal maturation of baroreflex heart rate control in neonatal swine.

OBJECTIVE: Despite extensive knowledge about basic baroreceptor function, there continues to be controversy as to whether there is postnatal maturation of the cardiovascular baroreflex. DESIGN/ANIMALS: Acutely studied postnatal developmental changes in baroreflex sensitivity with a neonatal porcine model in 28 chloralose-anesthetized piglets from birth to six weeks of age. INTERVENTIONS: Steady-state heart rate versus blood pressure response curves were generated by altering blood pressure with increasing doses of phenylephrine or nitroprusside. Data were fitted to the Hill equation for sigmoidal curves, and the maximum heart rate, maximum slope (sensitivity) and blood pressure at 50% maximal heart rate (P50) were calculated. MAIN RESULTS: Baroreflex sensitivity was found to increase from birth to six weeks of age (P < 0.0001), with the most rapid changes occurring after two weeks of age. Increasing age was accompanied by shift of the baroresponse curve to an increased range of heart rate changes at higher blood pressures. Maximal heart rates did not differ with advancing postnatal age. CONCLUSIONS: Swine baroreflex sensitivity increases from birth to six weeks of age, with higher blood pressures causing greater bradycardia in older piglets. These findings are consistent with postnatal maturation of the cardiovascular autonomic nervous system.

Age Factors↗
PubMed1993

Age-dependent changes of baroreflex efficiency in Dahl rats: effects of high salt intake.

The age-dependent changes in baroreflex control of heart rate were studied in inbred Dahl rats. At the age of 8 weeks the baroreflex slope was significantly greater in salt-resistant (R/Jr) than in salt-sensitive (S/Jr) rats fed a low-salt diet. The reverse was true in 16-week-old animals. High salt intake (8% NaCl diet for 4 weeks) suppressed baroreflex efficiency in both age groups of S/Jr animals whereas no effects occurred in R/Jr rats. Baroreflex slope was, however, significantly lower in young S/Jr rats with a severe form of salt hypertension than in adult salt-loaded S/Jr rats in which only a moderate blood pressure elevation was observed.

Aging↗
PubMed1993

Age-dependent changes of baroreflex efficiency in Dahl rats: effects of high salt intake.

The age-dependent changes in baroreflex control of heart rate were studied in inbred Dahl rats. At the age of 8 weeks the baroreflex slope was significantly greater in salt-resistant (R/Jr) than in salt-sensitive (S/Jr) rats fed a low-salt diet. The reverse was true in 16-week-old animals. High salt intake (8% NaCl diet for 4 weeks) suppressed baroreflex efficiency in both age groups of S/Jr animals whereas no effects occurred in R/Jr rats. Baroreflex slope was, however, significantly lower in young S/Jr rats with a severe form of salt hypertension than in adult salt-loaded S/Jr rats in which only a moderate blood pressure elevation was observed.

Aging↗
PubMed1995

A chronically instrumented rat model to assess the altered baroreflex due to exercise.

We developed a conscious, chronically instrumented, exercise-trained rat model and examined the time course of the training-induced alteration of baroreflex function in response to hypertensive conditions. Exercise-trained (ET) animals ran at 18 m.min-1, 15% grade, for 60 min.d-1, 5 d.wk-1 for 5 wk. Baroreflex tests were conducted on day 6 each week. Regression line slopes relating the change in mean arterial pressure (delta MAP) to the change in heart rate (delta HR) were used to assess baroreflex sensitivity. Intravenous injections of phenylephrine were used to create hypertensive conditions. Compared with the C group, slopes of ET animals were reduced (from 2.1 to 1.2 bpm.mm Hg-1, P < 0.05) as early as week 3 of training in response to increasing doses of PE, and reached 0.8 bpm.mm Hg-1 by the end of training. The reflex bradycardiac response (delta HR) to PE was reduced (P < 0.05) depending on the dose of PE and the duration of training: in micrograms PE.kg-1 body weight, 5 (71% +/- 6% of control at week 2), 3 (70% +/- 7% of control at week 3, and 1 (61% +/- 10% of control at week 4). The pressor (delta MAP) to PE remained constant throughout training. Thus, using a chronically instrumented rat model that maintains the ability to run, we observed that the ability of the arterial baroreflex to produce bradycardia during pressor events was substantially reduced following as few as 2 wk of training.

Animals↗
PubMed1996

Baroreflex modulation of the cardiovascular system: new insights from the joint analysis of blood pressure and heart rate signals.

This paper focuses on a number of methods for the analysis of the relationship between the arterial baroreflex and different components of blood pressure and heart rate variability. Broad-band spectral analysis techniques have allowed us to obtain experimental evidence that the arterial baroreflex exerts its influence not only on fast but also on slow components of blood pressure and heart rate, i.e., on components with periods longer than 60 sec. Focusing on faster changes in blood pressure and heart rate, both time domain and frequency domain techniques have been developed to track the sensitivity of baroreflex heart rate modulation over time, either in laboratory or in daily life conditions. These approaches have considerably broadened our understanding of the role of baroreflex modulation of the heart and peripheral circulation in a number of pathological and physiological conditions.

Animals↗
PubMed1996

Modulatory effects of nitric oxide on baroreflex activation in the brainstem nuclei of rats.

It has been shown that nitric-oxide (NO) was synthesized in the central nervous system as well as in vascular endothelial cells. We reported recently that nitric oxide was involved in central cardiovascular regulation of rat brainstem nuclei. In the present study, we evaluated further the baroreflex response of NO in the nucleus tractus solitarii (NTS) of rats. Male Sprague-Dawley rats were anesthetized with urethane, blood pressure and heart rate was monitored intra-arterially. Intramedullary microinjection (60 nl) of NO synthase inhibitor NG-methyl-L-arginine (L-NMMA), NG-nitro-L-arginine methyl ester(L-NAME) or normal saline was made into the NTS. Baroreflex response were elicited by increasing doses of phenylephrine (10-30 micrograms/Kg i.v.) before and after intra-NTS administration of L-NMMA, L-NAME or normal saline. The reflex bradycardia elicited by phenylephrine was significantly inhibited by the pretreatment of L-NMMA or L-NAME. Furthermore, the inhibitory effects on baroreflex activation by L-NMMA were significantly reversed by pretreatment with L-arginine. These results suggested that central endogenous NO was involved in the medullary regulation of blood pressure and that NO synthase inhibitor attenuated baroreflex activation.

Animals↗
PubMed1997

Baroreflex regulation of blood pressure during dynamic exercise.

From the work of Potts et al. Papelier et al. and Shi et al. it is readily apparent that the arterial (aortic and carotid) baroreflexes are reset to function at the prevailing ABP of exercise. The blood pressure of exercise is the result of the hemodynamic (cardiac output and TPR) responses, which appear to be regulated by two redundant neural control systems, "Central Command" and the "exercise pressor reflex". Central Command is a feed-forward neural control system that operates in parallel with the neural regulation of the locomotor system and appears to establish the hemodynamic response to exercise. Within the central nervous system it appears that the HLR may be the operational site for Central Command. Specific neural sites within the HLR have been demonstrated in animals to be active during exercise. With the advent of positron emission tomography (PET) and single-photon emission computed tomography (SPECT), the anatomical areas of the human brain related to Central Command are being mapped. It also appears that the Nucleus Tractus Solitarius and the ventrolateral medulla may serve as an integrating site as they receive neural information from the working muscles via the group III/IV muscle afferents as well as from higher brain centers. This anatomical site within the CNS is now the focus of many investigations in which arterial baroreflex function, Central Command and the "exercise pressor reflex" appear to demonstrate inhibitory or facilitatory interaction. The concept of whether Central Command is the prime mover in the resetting of the arterial baroreceptors to function at the exercising ABP or whether the resetting is an integration of the "exercise pressor reflex" information with that of Central Command is now under intense investigation. However, it would be justified to conclude, from the data of Bevegard and Shepherd, Dicarlo and Bishop, Potts et al., and Papelier et al. that the act of exercise results in the resetting of the arterial baroreflex. In addition, if, as we have proposed, the cardiopulmonary baroreceptors primarily monitors and reflexly regulates cardiac filling volume, it would seem from the data of Mack et al. and Potts et al. that the cardiopulmonary baroreceptor is also reset at the beginning of exercise. Therefore, investigations of the neural mechanisms of regulation involving Central Command and cardiopulmonary afferents, similar to those being undertaken for the arterial baroreflex, need to be established.

Animals↗
PubMed1998

Evidence of baroreflex adaptation to repetitive +Gz in fighter pilots.

BACKGROUND: The arterial baroreflex acts to maintain arterial pressure in the face of an orthostatic challenge. The high +Gz loads experienced by fighter pilots represent an extreme form of orthostatic challenge. G-induced loss of consciousness (G-LOC) represents a failure of the baroreflex system to maintain the appropriate level of cerebral perfusion. The anecdotal experience of fighter pilots is that their cardiovascular systems adapt to frequent exposure to high +Gz levels. HYPOTHESIS: The purpose of this study was to demonstrate that the baroreflex-mediated cardiovascular response of a group of 8 fighter pilots to a mild accelerative stimulus differs from that of a group of 12 non-pilots. METHODS: Arterial pressures and heart rate responses to rapid head-up tilting to +75 degrees were compared between the two groups. Five variables were examined: systolic, diastolic, mean arterial and pulse pressures, and heart rate. RESULTS: The cardiovascular responses of the groups were fundamentally different. In response to tilt, the non-pilots showed little change in systolic and mean arterial pressures, diastolic pressure increased slightly and pulse pressure decreased significantly. In the pilot group, however, significant increases were observed in systolic, diastolic and mean arterial pressures (p < 0.05), whereas pulse pressure did not change. Between groups there were significant differences observed in terms of arterial pressures (p < 0.05), but not heart rate. CONCLUSION: The baroreflex of a fighter pilot is capable of adapting to +Gz, becoming a more sensitive and effective BP control system as a result. This adaptation affords the pilot greater protection against G-LOC.

Adult↗
PubMed1985

Carotid baroreflex sensitivity and physical fitness in cycling tourists.

Carotid baroreceptors were stimulated with neck suction in 47 healthy subjects. Pulse interval lengthening was measured and the time course of the response was evaluated. Eight intensities of neck chamber suction were applied to select a criterion for computing the "RR response" that gives a significant linear relationship with the magnitude of the stimuli in the highest number of individuals. The best criterion was the maximal RR prolongation within 5 seconds after the onset of the stimulus. The slope of this relationship was defined as baroreflex sensitivity. The effect of physical fitness on baroreceptor function was investigated in 24 cycling tourists with a wide range of peak oxygen uptake and training characteristics. Baroreflex sensitivity averaged 7.3 +/- 0.8 msec X mm Hg-1 and was not significantly related to age, weight, basal heart rate, peak oxygen uptake and ventilation and other training characteristics. The results suggest that in man the so defined sensitivity of the carotid baroreflex control of heart rate is not influenced by the level of physical fitness and therefore the measurement of these characteristics can be neglected in evaluating baroreflex sensitivity.

Adolescent↗
PubMed1983

Renal sympathetic baroreflex during normoxia and during hypoxia in conscious and in anesthetized rabbits.

The responses of renal sympathetic nerve activity (RSNA) to changes in mean arterial pressure (MAP) during normoxia and hypoxia was studied in conscious rabbits and during anesthesia with pentobarbitone (PB) by determining the RSNA baroreflex curves. In conscious rabbits, the gain in RSNA response was greater and the range of MAP between minimum and maximum levels of RSNA was narrower than in anesthetized rabbits. The renal sympathetic baroreflex was augmented by hypoxia, indicating a central excitatory interaction between the effects of baro- and chemoreceptor stimulation. However, hypoxia produced no significant change in median blood pressure. During anesthesia with PB, resting MAP was decreased, median blood pressure was lowered, and renal sympathetic baroreflexes were less pronounced. Renal sympathetic baroreflex was augmented by hypoxia, and there was a significant increase in median blood pressure. These results provide direct evidence of an inhibitory effect of PB on the response of RSNA to baro- and chemoreceptor stimulation.

Anesthesia↗
PubMed1977

Baroreflex "resetting" by arterial hypoxia in the renal and cardiac sympathetic nerves of the rabbit.

1. Renal and cardiac sympathetic baroreflex functions were studied in sodium pentobarbitone anaesthetized rabbits given succinylcholine, during constant artificial ventilation with air and with hypoxic gas mixtures. Mean arterial pressure (MAP) was raised and lowered between values of 40 and 140 mm Hg by means of aortic and vena caval periovascular balloons and integrated sympathetic nerve activity (SNA) was recordered. 2. The relationship between MAP and SNA was sigmoid, with upper and lower plateau levels. The curves were defined by calculating median blood pressure, SNA Range and reflex gain. In both renal and cardiac sympathetics section of the carotid sinus and aortic nerves completely abolished the MAP-related changes in SNA. 3. The renal baroreflex curves were reset from control levels during hypoxia. Median blood pressure increased, as did SNA Range and gain. These effects were due to central interactions between arterial baroreceptor, arterial chemoreceptor and vagal afferent activity. 4. The cardiac sympathetic baroreflex curves were shifted in the opposite direction from control with reduction in median blood pressure, SNA Range and reflex gain. These changes were due to chemoreceptor-arterial baroreceptor interactions. 5. Arterial hypoxia thus evokes a differentiated pattern of baroreflex resetting in the renal and cardiac sympathetic montoneuron pools with differing changes in neural response range and sensitivity to arterial pressure changes.

Animals↗
PubMed1997

[Problems in carrying out baroreflex sensitivity measurements in clinical routine practice: practicability and complications].

Measurement of baroreflex sensitivity is a new method to identify patients after myocardial infarction with a high risk for sudden cardiac death, ventricular tachycardia or ventricular fibrillation. In this retrospective study the baroreflex sensitivity was obtained noninvasively by measuring the systolic blood pressure blood pressure with a FINAPRES-device and correlating this with the R-R intervals of the ECG after raising blood pressure with an intravenous dose of Norfenefrin-hydrochloride (Novadral). According to other investigators a correlation of > 0.7 with a significance of p < 0.05 was recommended for evaluable results with a baroreflex sensitivity < 3 ms/mm Hg being judged as decreased. We investigated 302 patients (mean age 59 +/- 17 years, 224 males, 78 females). 75% of the investigations showed acceptable results. In 77 cases (25%) reasonable results could not be achieved. We found premature ventricular beats to be responsible in 18 investigations (6% of all investigations). 41 (13.1%) of all investigations were not evaluable because of bad correlation for unknown reason. When we looked closely at these nonevaluable results, we found a significantly higher number of patients with impaired left ventricular ejection fraction (< 40%), diabetes or inducible sustained ventricular tachyarrhythmia in the electrophysiologic study in this group. During all investigations no severe side effects were observed. We conclude that the noninvasive measuring of the baroreflex sensitivity is a save method and leads to reasonable results in 75% of the investigations. In 13.1% it is not possible for unknown reason to achieve sufficiently correlating values. These measurements cannot be evaluated from nowadays' standards and have to be further investigated as they may indicate a population at high risk.

Adult↗
PubMed1993

Fentanyl antagonizes diazepam on carotid sinus baroreflex control of circulation in rabbits.

To investigate the effects of a combination of fentanyl and diazepam on carotid sinus baroreflex in conscious rabbits, we examined the responses of mean systemic arterial pressure (MAP), heart rate (HR) and total peripheral resistance (TPR) to bilateral carotid occlusion (BCO). Seven rabbits were given 0.5 mg.kg(-1) of diazepam i.v. followed by 10 mg.kg(-1) of fentanyl i.v. at 5 min intervals (group 1), and the drugs were given in the reverse order to 5 other rabbits (group 2). BCO was repeated in conscious state (control) and after each drug injection. MAP responses did not differ from control response in either group when both drugs were given. In group 1, however, diazepam decreased HR response to 71.4% of control, and increased TPR response by 36%. Fentanyl administration reversed diazepam-induced changes in BCO responses to the control level. In group 2, fentanyl decreased TPR response to 61.6% of control and increased HR response by 41.5%. Administration of diazepam following fentanyl restored HR and TPR responses to control levels. Carotid sinus baroreflex gain was 3.1 +/- 0.4 (mean +/- SEM) in control and 3.1 +/- 0.4 after administration of both drugs in 12 rabbits. The results suggest that a sedative dose of either fentanyl or diazepam antagonizes the other drug's action on the carotid sinus baroreflex. The combination of fentanyl and diazepam has little influence on carotid sinus baroreflex control of the circulation in rabbits.

Journal Article↗
PubMed1988

Preservation of baroreflex control of vascular resistance under ketamine anesthesia in rats.

The aim of this study was to examine the effects of ketamine and pentobarbital on the baroreceptor reflex control of vascular resistance in rats. The gains of baroreflex were assessed by relating changes in arterial pressure to changes in hindlimb perfusion pressure, using an extracorporeal perfusion circuit with a delay system. Reflex-induced vasodilation or vasoconstriction in response to a rise or a fall in arterial pressure were elicited by injections of phenylephrine or nitroprusside, respectively. The gains of baroreflex were not altered by ketamine 1 and 5 mg/kg (i.v.), whereas those were depressed by pentobarbital 5 mg/kg (i.v.). The results suggest that ketamine preserves the baroreflex control of vascular resistance and pentobarbital depresses it. The preservation of the baroreflex control of vascular resistance may be advantageous for patients with hypovolemia to sustain the blood pressure.

Journal Article↗
PubMed1983

Autonomic and baroreflex function after captopril in hypertension.

Absent reflex tachycardia with captopril therapy suggests blunting of circulatory reflexes, perhaps contributing to antihypertensive efficacy, and angiotensin converting enzyme inhibition may alter sympathetic function. Captopril effects on autonomic function were investigated in five severe hypertensive patients. Mean blood pressure fell in all patients (from 141 +/- 6 to 119 +/- 7 mm Hg, p less than 0.02) without orthostatic blood pressure fall or increase in heart rate (both p greater than 0.1) on captopril. Captopril did not alter baroreflex sensitivity as tested by amyl nitrile hypotension or phenylephrine hypertension (both p greater than 0.1). Comparison of these severely hypertensive patients to age matched normotensive control subjects did reveal markedly blunted baroreflex sensitivity in both the amyl nitrite test (by 89%, p less than 0.01) and the phenylephrine test (by 83%, p less than 0.01), suggesting that baseline blunting of baroreflex function may in part account for absence of reflex tachycardia. Captopril diminished the cardioacceleration after cold stress (from 61 +/- 38 to 23 +/- 43 msec, p less than 0.05) as well as the blood pressure fall after alpha-adrenergic blockade (from 46 +/- 13 to 24 +/- 9 mm Hg, p less than 0.05), suggesting diminished sympathetic stimulation of resistance vessels and decreased sympathetic participation in blood pressure maintenance, possibly at the prejunctional synaptic level. Four biochemical indices of sympathetic activity did not change. Thus captopril-treated patients had blunted reflex tachycardia, commensurate with blunted baroreflex function at baseline, and physiologic and pharmacologic evidence of diminished sympathetic activity was obtained with captopril therapy. Whether diminished sympathetic activity is involved in captopril's antihypertensive effect has not been determined.

Aged↗