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PubMed2002

Ablation of NK1 receptors in rat nucleus tractus solitarii blocks baroreflexes.

The neuropeptide substance P (SP) is found in vagal afferent nerves within the nucleus tractus solitarii, where it is released on stimulation of arterial baroreflexes. The neurokinin-1 receptors at which SP may act have been identified in the nucleus tractus solitarii, but there remains uncertainty if the neurons at which SP acts are critical to baroreflex transmission. By using SP conjugated with the toxin saporin, which kills the neurons at which SP may act, we sought to test the hypothesis that neurons expressing the neurokinin-1 receptor are critical to baroreflex transmission in the nucleus tractus solitarii. One and 2 weeks after injection of the toxin into the rat nucleus tractus solitarii, immunoreactivity for the neurokinin-1 receptor was lost. When the toxin had been injected bilaterally, the baroreflex gain was significantly reduced. Therefore, neurons that express SP receptors play a critical role in mediating baroreflexes through the nucleus tractus solitarii of rat.

Animals↗
PubMed2005

Exercise training improves baroreflex sensitivity associated with oxidative stress reduction in ovariectomized rats.

The protection from coronary events that young women have is sharply reduced at menopause. Oxidative stress and baroreflex sensitivity impairment of the circulation have been demonstrated to increase cardiovascular risk. On the other hand, exercise training has been indicated as a nonpharmacological treatment for many diseases. The aim of the present study was to test the hypothesis that exercise training can improve baroreflex sensitivity associated with reduction in oxidative stress in ovariectomized rats, an experimental model of menopause. Exercise training was performed on a treadmill for 8 weeks. Arterial pressure and baroreflex sensitivity, which were evaluated by tachycardic and bradycardic responses to changes in arterial pressure, were monitored. Oxidative stress was evaluated by chemiluminescence and superoxide dismutase and catalase antioxidant enzyme activities. Exercise training reduced resting mean arterial pressure (112+/-2 vs 122+/-3 mm Hg in the sedentary group) and heart rate (325+/-4 vs 356+/-12 bpm in the sedentary group) and also improved baroreflex sensitivity (tachycardic response, 63% and bradycardic response, 58%). Myocardium (25%) and gastrocnemius muscle (48%) chemiluminescence were reduced, and myocardial superoxide dismutase (44%) and gastrocnemius catalase (97%) activities were enhanced in trained rats in comparison with sedentary rats. Myocardium chemiluminescence was positively correlated with systolic arterial pressure (r=0.6) and inversely correlated with baroreflex sensitivity (tachycardic response, r=-0.8 and bradycardic response, r=-0.7). These results indicate that exercise training in ovariectomized rats improves resting hemodynamic status and reflex control of the circulation, probably associated with oxidative stress reduction, suggesting a homeostatic role for exercise training in reducing cardiovascular risk in postmenopausal women.

Animals↗
PubMed2005

Impaired heart rate baroreflex in older rats: role of endogenous angiotensin-(1-7) at the nucleus tractus solitarii.

Age-related baroreflex reductions in function may originate from central neural dysregulation as well as vascular structural/functional changes. We determined the role of 2 angiotensin (Ang) peptides at the nucleus tractus solitarii in age-related baroreflex impairment. Baroreflex sensitivity control of heart rate in response to increases in blood pressure was tested in younger (3 to 5 months) and older (16 to 20 months) anesthetized male Sprague-Dawley rats before and after bilateral solitary tract injections of the Ang II type 1 (AT1) receptor antagonist candesartan (24 pmol) or the Ang-(1-7) antagonist (D-Ala7)-Ang-(1-7) (144 fmol or 24 pmol). Basal reflex sensitivity of older rats was significantly lower than younger rats. In younger rats, the reflex was facilitated by bilateral candesartan injections and attenuated by bilateral (D-Ala7)-Ang-(1-7) injections. In older rats, the reflex was facilitated by AT1 blockade; however, (D-Ala7)-Ang-(1-7) injected into the solitary tract nucleus had no effect. Neprilysin mRNA in the medulla was lower in older rats compared with younger rats, whereas angiotensin-converting enzyme (ACE), ACE2, and mas receptor mRNA levels of older rats did not differ from values of younger rats. Thus, opposing actions of endogenous Ang II and Ang-(1-7) in the solitary tract nucleus contribute to baroreflex function in response to increases in mean arterial pressure of younger rats. The attenuated counterbalancing effect of Ang-(1-7) on baroreflex function is lost in older rats, which may be attributable to diminished production of the peptide from neprilysin.

Aging↗
PubMed1994

Baroreflex failure in a patient with central nervous system lesions involving the nucleus tractus solitarii.

Animal studies have shown the importance of the nucleus tractus solitarii, a collection of neurons in the brain stem, in the acute regulation of blood pressure. Impulses arising from the carotid and aortic baroreceptors converge in this center, where the first synapse of the baroreflex is located. Stimulation of the nucleus tractus solitarii provides an inhibitory signal to other brain stem structures, particularly the rostral ventrolateral medulla, resulting in a reduction in sympathetic outflow and a decrease in blood pressure. Conversely, experimental lesions of the nucleus tractus solitarii lead to loss of baroreflex control of blood pressure, sympathetic activation, and severe hypertension in animals. In humans, baroreflex failure due to deafferentation of baroreceptors has been previously reported and is characterized by episodes of severe hypertension and tachycardia. We present a patient with an undetermined process of the central nervous system characterized pathologically by ubiquitous infarctions that were particularly prominent in the nucleus tractus solitarii bilaterally but spared the rostral ventrolateral medulla. Absence of a functioning baroreflex was evidenced by the lack of reflex tachycardia to the hypotensive effects of sodium nitroprusside, exaggerated pressor responses to handgrip and cold pressor test, and exaggerated depressor responses to meals and centrally acting alpha 2-agonists. This clinicopathological correlate suggests that the patient's baroreflex failure can be explained by the unique combination of the destruction of sympathetic inhibitory centers (ie, the nucleus tractus solitarii) and preservation of centers that exert a positive modulation on sympathetic tone (ie, the rostral ventrolateral medulla).

Adult↗
PubMed1995

Brain 'ouabain' and desensitization of arterial baroreflex by high sodium in Dahl salt-sensitive rats.

In Dahl salt-sensitive (S) rats, high sodium intake further desensitizes arterial baroreflex function. To assess the possible involvement of brain "oubain," we gave Dahl S rats a regular or high sodium diet from 4 to 7 weeks of age and administered intracerebroventricular antibody Fab fragments, which bind ouabain with high affinity, or gamma-globulins as control (200 micrograms/12 microL per day for both) using osmotic minipumps. We assessed arterial baroreflex function by plotting changes in renal sympathetic nerve activity or heart rate against changes in mean arterial pressure of conscious rats elicited by intravenous phenylephrine and nitroprusside. Dahl S rats on high sodium treated with gamma-globulins showed a significantly higher resting mean arterial pressure versus other rats (130 to 140 versus 95 to 105 mm Hg). In rats treated with gamma-globulins, high sodium desensitized baroreflex control of renal sympathetic nerve activity compared with rats on regular sodium (average gain: -1.88 +/- 0.12 versus -2.73 +/- 0.13, P < .05). In contrast, in rats treated with Fab fragments, high sodium did not increase blood pressure and did not desensitize but slightly sensitized reflex control of renal sympathetic nerve activity. Changes in reflex control of heart rate were similar to those of renal sympathetic nerve activity. These data indicate that blockade of brain "oubain" prevents sodium-induced hypertension as well as the desensitization of the arterial baroreflex in Dahl S rats. Increased brain "oubain" may desensitize the arterial baroreflex and thereby facilitate the hypertension in Dahl S rats on high sodium.

Animals↗
PubMed1997

Improvement in baroreflex function by an oral angiotensin receptor antagonist in rats with myocardial infarction.

Impaired baroreflex function is a factor responsible for poor prognosis in myocardial infarction patients. Using logistic function curves, we calculated the maximal gain of the baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate in conscious Wistar-Kyoto and spontaneously hypertensive rats whose left anterior descending artery had been ligated 4 weeks earlier. We further investigated whether 3-week oral treatment with the angiotensin II type 1 receptor antagonist TCV-116 would improve the baroreflex in rats with myocardial infarction. The maximal gain of the mean arterial pressure-RSNA relation in spontaneously hypertensive rats with myocardial infarction and treated with vehicle (1.7 +/- 0.1% control per mm Hg) was smaller than the gain in sham-operated hypertensive rats (2.3 +/- 0.1% control per mm Hg). After 3-week oral treatment with TCV-116, the maximal gain of the arterial pressure-RSNA relation in hypertensive rats with myocardial infarction was 2.3 +/- 0.1% control per mm Hg and significantly greater than the gain in infarcted and vehicle-treated hypertensive rats. In hypertensive rats, the maximal gain of the arterial pressure-heart rate relation of infarcted and TCV-116-treated rats was larger than in infarcted and vehicle-treated rats but significantly smaller than in sham-operated rats. These results demonstrate that oral treatment with an angiotensin receptor antagonist is effective in restoring the impaired baroreflex caused by myocardial infarction and that endogenous angiotensin II is one of the critical factors involved in the impaired baroreflex in myocardial infarction.

Administration, Oral↗
PubMed1997

Sympathoexcitatory response to cyclosporin A and baroreflex resetting.

We postulate that the sympathoexcitatory response associated with the immunosuppressive agent cyclosporin A is due to an upward resetting of the arterial baroreflex. We performed studies in conscious intact and sinoaortic-denervated rabbits instrumented with catheters and renal nerve electrodes. In intact rabbits, cyclosporin A (20 mg/kg i.v., 30 minutes) produced significant increases in renal sympathetic nerve activity (100% to 269 +/- 74%, P < .05) but did not increase mean arterial pressure. In intact rabbits, we determined arterial baroreflex curves relating renal sympathetic nerve activity and heart rate to mean arterial pressure by producing ramp increases (intravenous phenylephrine) and decreases (intravenous nitroprusside) in mean arterial pressure. Cyclosporin A treatment produced a shift of the midrange of the baroreflex control of heart rate (78.0 +/- 4.1 to 84.6 +/- 4.7 mm Hg, P < .05) and renal sympathetic nerve activity (74.6 +/- 3.9 to 87.0 +/- 4.8 mm Hg, P < .05). Vehicle administration produced no effects on arterial baroreflex curves relating renal sympathetic nerve activity and heart rate to mean arterial pressure. Compared with vehicle treatment, cyclosporin A reduced the maximum gain of heart rate (-5.6 +/- 0.6 versus -3.1 +/- 0.8 beats per minute per millimeter of mercury, P < .05) but had no effect on the maximum gain of renal sympathetic nerve activity. In conscious sinoaortic-denervated rabbits, cyclosporin A had no effect on mean arterial pressure (95.7 +/- 7.3 to 91.8 +/- 10.8 mm Hg), renal sympathetic nerve activity (100% to 110 +/- 6%). and heart rate (287 +/- 10 to 279 +/- 8 beats per minute). However, when the same sinoaortic-denervated rabbits were anesthetized with sodium pentobarbital, cyclosporin A (20 mg/kg i.v.) produced increases in renal sympathetic nerve activity (100% to 189 +/- 27%). These data indicate (1) that the sympathoexcitatory response to cyclosporin A depends on baroreceptor afferent input in the conscious state and (2) that this response involves an upward resetting of the arterial baroreflex.

Animals↗
PubMed1997

Baroreflex sensitivity assessed by complex demodulation of cardiovascular variability.

We used complex demodulation of cardiac interval and systolic arterial blood pressure oscillations in the low-frequency band (0.04 to 0.14 Hz) to investigate baroreceptor control of heart rate. Baroreflex sensitivity was defined as the instantaneous amplitude of complex-demodulated oscillations in the RR interval divided by the instantaneous amplitude of complex-demodulated oscillations in systolic blood pressure. We evaluated the method using both simulated and actual data obtained from 33 healthy nonsmokers during supine and standing postures. To test the validity and reliability of the method, we compared the mean values of baroreflex sensitivity calculated using complex demodulation with the values obtained using power spectral analysis and sequential analysis of spontaneous variations in blood pressure and RR interval. All three methods applied to the simulated data yielded the same values of baroreceptor sensitivity. Mean values of baroreflex sensitivity assessed by complex demodulation of the actual data were similar to those calculated by both power spectral analysis and sequential analysis (13.9 +/- 5.2 versus 13.7 +/- 6.7 or 14.3 +/- 6.5 ms/mm Hg for supine and 7.3 +/- 2.8 versus 7.0 +/- 3.0 or 7.2 +/- 2.8 ms/mm Hg for standing, respectively). In addition, a significant correlation existed between the values obtained by complex demodulation and power spectral analysis (r = .97, P = .0001) and sequential analysis (r = .98, P = .0001). Furthermore, complex demodulation-derived baroreflex sensitivity fluctuated across time during both the supine and standing postures, and this could not be discerned by power spectral analysis. The results indicate that complex demodulation provides a dynamic assessment of baroreflex sensitivity and may be a useful tool in exploring reflex autonomic control of the cardiovascular system.

Adult↗
PubMed1997

Malignant vagotonia due to selective baroreflex failure.

Baroreflex failure is characterized by dramatic fluctuations of sympathetic activity and paroxysms of hypertension and tachycardia. In contrast, unopposed parasympathetic activity has not been described in patients with baroreflex failure because of concurrent parasympathetic denervation of the heart. We describe the unusual case of a patient with baroreflex failure in a setting of preserved parasympathetic control of HR manifesting episodes of severe bradycardia and asystole. Thus, parasympathetic control of the HR may be intact in occasional patients with baroreflex failure. Patients with this selective baroreflex failure require a unique therapeutic strategy for the control of disease manifestations.

Baroreflex↗
PubMed2000

Mental stress-induced increase in blood pressure is not related to baroreflex sensitivity in middle-aged healthy men.

The baroreflex that acts to blunt blood pressure (BP) variations through opposite variations in heart rate should limit the BP increase produced by an emotional challenge. However, relations between baroreflex sensitivity and BP reactivity induced by a psychological stress in a large group of adults have never been firmly established. In 280 healthy men, rest (10 minutes) and stress (5 minutes) BP and heart rate were recorded beat to beat by a blood pressure monitor. The mental stress was elicited by a well-standardized computerized version of a word color conflict stress test (Stroop Color Test). Rest and stress baroreflex sensitivity was assessed by the cross-spectral analysis of BP and heart rate and by the sequence method. The stress-induced increase in systolic BP (22.4+/-0.1 mm Hg) was not correlated with resting baroreflex sensitivity but was slightly correlated (r=0.2, P<0.001) with BP variability assessed either by standard deviation or by mid-frequency band spectral power. Our results suggested that a centrally mediated sympathetic stimulation overcame cardiac autonomic regulation and emphasized the role of the sympathetic vasoconstriction in the pressure response at the onset of the stressing stimulation. During the sustained sympathoexcitatory phase, the cardiac baroreflex blunts BP variations but at a lower sensitivity.

Adolescent↗
PubMed2006

Effects of sevoflurane anesthesia on carotid-cardiac baroreflex responses in humans.

Sevoflurane depresses cardio-vagal baroreflex gain (ability of vagally mediated R-R interval response to arterial blood pressure change). We examined the effects of sevoflurane anesthesia on maximum buffering capacity of vagally mediated hemodynamic control (baroreflex range) by examining the entire stimulus-response baroreflex relation. Electrocardiogram and invasive arterial blood pressure were monitored in 11 healthy volunteers. Carotid-cardiac baroreflex responses were elicited by increasing neck chamber pressure (external pressure applied over the bilateral carotid sinuses) to 40 mm Hg for 5 heartbeats followed by decreasing chamber pressure by successive 15-mm Hg R-wave triggered decrements to -65 mm Hg during held expiration. R-R intervals were plotted as functions of preceding carotid distending pressure. Range, maximum gain, and operational point (relative position of the resting set point within the entire baroreflex response curve) were determined at conscious baseline, during 2% (end-tidal) sevoflurane anesthesia, without and with phenylephrine infusion to maintain conscious arterial blood pressure, and at 30, 60, 120, and 180 min after emergence from anesthesia. Sevoflurane anesthesia significantly depressed maximum gain (from 3.84 +/- 0.99 to 1.04 +/- 0.40 ms/mm Hg [mean +/- sd]; P < 0.001) and range (from 207 +/- 43 to 52 +/- 19 ms; P < 0.001) of the reflex relation, both of which recovered at 120 and 180 min after emergence. Phenylephrine infusion only partially restored these variables. The operational point was unchanged throughout the study. Our results indicate that maximum cardio-vagal compensatory response to buffer hemodynamic perturbation is depressed during sevoflurane anesthesia. Sevoflurane-induced hypotension, which produced vagal withdrawal, did not play an important role in depressing cardio-vagal reflex function.

Adult↗
PubMed1996

Modifications of arterial baroreflexes: obligatory roles in cardiovascular regulation in stress and poststress recovery.

Despite the physiological importance of arterial baroreflexes as a powerful stabilizer of blood pressure, their functions themselves are not always stable and there are a variety of circumstances in which they are significantly modulated. During stressful conditions, including fight/flight, defense/attack, somatic nociception, visceral nociception, exercise, and mental stress, arterial baroreflexes are generally inhibited. The inhibition is purposeful for achieving dynamic readjustment of circulation needed for the animal's reaction to cope with these conditions. Central sites which are proposed to be involved in the inhibition include the motor cortex, amygdala, hypothalamus, dorsolateral part of the periaqueductal gray matter, parabrachial nucleus, cerebellar vermis, etc. On the other hand, arterial baroreflexes are occasionally facilitated, during sleep, following endurance exercise, etc. The facilitation favors restoration of energy exhausted during a stressful phase in which the animal reacts actively to changing environment. The central sites proven to elicit the facilitation are the medial prefrontal cortex, the preoptic/anterior hypothalamus, the ventrolateral part of the periaqueductal gray matter, and the nucleus raphe magnus. The inhibition and facilitation of arterial baroreflexes, which probably occur alternatively, are essential mechanisms supporting reactions to stressful conditions and poststress recovery, respectively. This review describes when, how, and why the arterial baroreflexes are so modulated.

Animals↗
PubMedDate not supplied

Angiotensin II-dependent hypertension and the arterial baroreflex.

Angiotensin II (ANG II)-dependent hypertension involves the resetting of the heart rate (HR) and sympathetic baroreflex toward higher pressures in conscious rabbits. The resetting of the HR baroreflex function occurs within minutes of the administration of ANG II, while the resetting of the sympathetic baroreflex requires several days. In conscious rabbits, an intact area postrema (AP) is required for the resetting of either the HR or sympathetic baroreflex function. Data is also presented showing that pretreatment with an alpha-1 adrenergic receptor antagonist prevents the early resetting of the HR baroreflex.

Angiotensin II↗
PubMed1996

Effects of antidotes to cocaine on the deregulation of the baroreflex by the alkaloid.

Cocaine exerts in the rat an inhibitory effect on the baroreflex induced by bilateral clamping of the carotid arteries. The present series of experiments were designed to test the effectiveness of cocaine antidotes on this deregulation of the baroreflex. Sprague-Dawley rats were fitted under pentobarbital anesthesia with a catheter in the caudal artery, and their carotid arteries were exposed. The pressure signal from the caudal artery was treated on line by a microcomputer for continuous display of blood pressure and heart rate measurements. The animals were administered intraperitoneally either 50 mg cocaine or an equal volume of saline. Five minutes later, they were administered either saline or proven antidotes to cocaine (diltiazem, nicardipine, enzyme converting inhibitor [ECI], enalaprilat associated with diazepam). After 2 min, stimulation of the baroreceptor was performed by bilateral clamping of the two carotids for a period of 2 min. The measures of the maximal variation in systolic pressure before and after clamping indicated a significant difference between saline and cocaine treated animals (P < 0.05), with the former displaying a much greater increment in blood pressure after clamping. The cocaine-treated animals, administered diltiazem, nicardipine, and ECI associated with diazepam, presented after clamping of the carotid arteries a normal baroreflex with increments in blood pressure not significantly different from those occurring in the animals receiving saline, but significantly different from those administered cocaine only (P < 0.05). Baroreflex deregulation by cocaine may also be restored by an angiotensin II receptor antagonist. The possible role of this peptide in mediating in part baroreflex activity is discussed.

Analysis of Variance↗
PubMed2000

Clinical evaluation of arterial baroreflex activity in diabetes.

The clinical and prognostic relevance of the evaluation of the arterial baroreflex is now firmly established in clinical cardiology, where a number of important studies have shown that impairment of arterial baroreflex has independent adverse prognostic value. The results, applied to diabetes, have generated a new perspective in our understanding of autonomic neuropathy. Available data indicate that in diabetes, with or without overt autonomic neuropathy, a widespread abnormality in the baroreflex function is a common finding. This abnormality is evident not only at the cardiac level, but also at the vascular level, by using new techniques able to provide more complete information on the direct baroreflex modulation of the resistance vessels. The question of whether this abnormality is already the consequence of neural damage or only the consequence of a functional involvement remains unsettled, although animal studies and the presence of widespread baroreflex abnormalities even in asymptomatic subjects tend to support the view that baroreceptor function can be altered due to functional and, later, structural damages of efferent nerves, involving both branches of the autonomic nervous system.

Animals↗
PubMed1999

[Bradykinin inhibits carotid sinus baroreflex in anesthetized rats].

The effects of bradykinin (BK) on the carotid baroreflex were examined in 36 anesthetized rats with isolated carotid sinus perfusion. The results obtained are as follows. (1) By perfusing the isolated carotid sinus with BK (1.0 mumol/L), the functional curve of baroreflex was shifted to the right and upward, its peak slope (PS) decreasing from 0.44 +/- 0.14 to 0.31 +/- 0.01 kPa (P < 0.01) and the reflex decrease in mean arterial pressure (RD) was lowered from 6.85 +/- 0.18 to 4.46 +/- 0.16 kPa (P < 0.05), while the threshold pressure (TP), equilibrium pressure (EP) and saturation pressure (SP) were significantly enhanced from 7.76 +/- 0.20 to 10.04 +/- 0.09 kPa (P < 0.001), 12.72 +/- 0.29 to 13.74 +/- 0.31 kPa (P < 0.05) and 23.28 +/- 0.24 to 25.31 +/- 0.20 kPa (P < 0.01), respectively. Among the functional parameters of carotid baroreflex, the changes in RD, PS and TP induced by BK were dose-dependent. (2) By pretreatment with indomethacin (10 mumol/L), an inhibitor of prostaglandin synthesis, the above-mentioned effects of BK on carotid baroreflex were not affected. (3) Preperfusion with an inhibitor of NO synthase L-NAME (100 mumol/L) could completely eliminate the effects of BK. (4) Pretreatment with angiotensin-converting enzyme inhibitor captopril (20 mumol/L) could potentiate the effects of BK. Taken together, it is indicated that BK may cause vascular endothelium to release NO, thereby inhibiting the carotid baroreflex.

Animals↗
PubMed2001

Mechanics of the carotid artery wall and baroreflex sensitivity after acute ethanol administration in young healthy volunteers.

The effects of ethanol administered orally (300 mg/kg in 250 ml of water) or intravenously (7.5 mg.min(-1).kg(-1) in 250 ml of saline over 40 min) on common carotid haemodynamics, wall mechanics and baroreflex sensitivity were compared with the effects of the intravenous infusion of 250 ml of saline. Ethanol or saline was administered to 10 healthy volunteers after 30 min of supine rest, and measurements were obtained 40 min (median; range 34-46 min) after administration. After ethanol administration, the plasma alcohol level rose from 0 to 0.3+/-0.07 g/l. Mean arterial blood pressure had risen slightly at 20 min, but was normalized by 40 min, the time at which the haemodynamic study was performed. Heart rate decreased after infusion of either saline or alcohol, but was unchanged after oral ethanol administration. Both oral and intravenous ethanol administration were associated with significant decreases in baroreflex sensitivity, carotid shear stress and blood velocity, compared with resting values, while the mean carotid artery diameter was increased, and blood viscosity and mean blood flow were unchanged. No changes were observed in these parameters after saline administration. Ethanol, administered either intravenously or orally, increased the stiffness of the carotid artery and decreased the pulsatility (systo-diastolic changes) of its diameter. A direct, statistically significant correlation was found between the decrease in shear stress and the decrease in baroreflex heart rate control sensitivity after both modes of alcohol administration, while no such correlation was found between the increase in the Peterson elastic modulus and the decrease in carotid diameter pulsatility on the one hand or the decrease in baroreflex sensitivity on the other. In conclusion, reduced shear stress associated with vasodilatation of the carotid artery wall may contribute to the decrease in baroreflex sensitivity observed after acute ethanol administration.

Administration, Oral↗
PubMed1997

Baroreflex during exercise in different postures before and after 20-days bed rest.

Vagal-cardiac baroreflex functions in young healthy humans (n=6) were investigated in four different conditions; supine rest, seated rest, supine and seated exercise (50 watts) before and after 20-day horizontal bed rest. By selectively stimulating carotid baroreceptors using a neck pressure and suction technique, the primary finding was that the baroreflex sensitivity tuation at which we observed a tendency for an attenuation (0.05<p<0.07) of baroreflex sensitivity. The range of decrease in heart rate during neck suction was diminished (p<0.05) after bed rest, but only during supine rest. In conclusion, an attenuation of carotid vagal baroreflex after inactivity was found to be dependent on posture, and was found only in supine rest. It was also concluded that an exaggerated exercise tachycardia found after bed rest is not due to an attenuation of vagal carotid baroreflex sensitivity in itself.

Adult↗