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PubMed1998

Role of 17beta-estradiol in the modulation of baroreflex sensitivity in male rats.

Female mammals have an enhanced baroreflex sensitivity compared with their male counterparts, leading researchers to speculate that estrogen modulates autonomic tone. Therefore, this study tests the hypothesis that exogenous estrogen can enhance the baroreflex sensitivity of male rats. Male Sprague-Dawley rats anesthetized with thiobutabarbitol sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate and for the intravenous injection of drugs. The baroreflex was tested using intravenous injections of phenylephrine (0.025, 0.05, and 0.1 mg/kg), and the cardiovascular responses were plotted to obtain a measure of the sensitivity of the cardiac baroreflex. Intravenous injection of estrogen produced dose-related increases in the baroreflex sensitivity due to an increase in the magnitude of the reflex bradycardia. In a separate group of animals, stimulation of the vagus nerve for 2 h resulted in a decrease in baroreflex sensitivity. This effect was blocked when estrogen (1 x 10(-2) mg/kg) was administered immediately before the end of stimulation. In conclusion, intravenous injection of estrogen in male rats significantly enhanced baroreflex sensitivity and blocked the attenuation in the baroreflex sensitivity observed after vagal stimulation.

Animals↗
PubMed1999

Vasopressin V2 receptor enhances gain of baroreflex in conscious spontaneously hypertensive rats.

The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using novel nonpeptide AVP V1- and V2-receptor antagonists. Baroreceptor heart rate (HR) reflex was investigated in both SHR and WKY rats which were intravenously administered the selective V1- and V2-receptor antagonists OPC-21268 and OPC-31260, respectively. Baroreflex function was assessed by obtaining alternate pressor and depressor responses to phenylephrine and sodium nitroprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous administration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V1-receptor antagonist had no significant effect on resting MAP or HR values or on baroreflex parameters in both groups of rats, although this dose was shown to significantly inhibit the pressor response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V2-receptor antagonist significantly attenuated the gain (or slope) of the baroreflex curve (to 73 +/- 3 and 79 +/- 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pressor responses were also attenuated with the higher dose of the V2-receptor antagonist. These findings suggest that AVP tonically enhances baroreflex function through a V2 receptor in the SHR.

Animals↗
PubMed1993

Effect of exercise on autonomic mechanisms of baroreflex control of heart rate.

We tested whether moderate dynamic exercise alters baroreflex control of heart rate (HR) in conscious dogs and whether the autonomic mechanisms mediating arterial baroreflex control of HR differ in the two settings of rest and exercise. Conscious, chronically instrumented dogs were studied during rest and moderate treadmill exercise (6.4 kpm, 10% grade). Sustained changes in mean arterial pressure (MAP) were induced by graded intravenous infusions of phenylephrine and nitroglycerine. Baroreflex HR sensitivity was assessed as the slope of the linear regression between MAP and HR. Responses to increases and decreases in MAP were analyzed separately. Studies were repeated after muscarinic (atropine, 0.2 mg/kg iv) or beta-adrenergic (propranolol, 2.0 mg/kg iv) blockade during rest and exercise. During control experiments both at rest and during exercise, baroreflex changes in HR were greater in response to decreases than to increases in MAP. Experiments performed after separate cardiac autonomic blockade revealed that at rest baroreflex-induced bradycardia occurs via parasympathetic activation but tachycardia occurs via a combined parasympathetic inhibition-sympathetic activation. During exercise, whereas the magnitude of baroreflex responses was unchanged compared with rest, the autonomic mechanisms mediating the baroreflex changes in HR were altered. In this setting, baroreflex tachycardia and bradycardia occur via modulation of both parasympathetic and sympathetic tone.

Adrenergic beta-Antagonists↗
PubMed2003

Baroreflex buffering is reduced with age in healthy men.

BACKGROUND: Baroreflex buffering is an important mechanism in arterial blood pressure control. The effect of healthy (physiological) aging on tonic baroreflex buffering in humans is unknown. METHODS AND RESULTS: Baroreflex buffering was determined in 27 young (aged 25+/-1 years) and 16 older (aged 65+/-1 years) healthy normotensive men by measuring the potentiation of the systolic blood pressure (SBP) responses to a phenylephrine bolus (BRBbolus) and incremental infusion (BRBslope) during compared with before ganglionic blockade with trimethaphan. The SBP responses to phenylephrine either were not different or greater in the older men before ganglionic blockade, but smaller during ganglionic blockade. BRBbolus (2.1+/-0.4 versus 5.1+/-0.7, P<0.001) and BRBslope (1.6+/-0.2 versus 3.5+/-0.4, P<0.0001) were approximately 115% smaller in the older men. Baroreflex buffering was not consistently related to mean levels or variability of blood pressure or heart rate, or to cardiovagal baroreflex sensitivity, but correlated with muscle sympathetic nerve activity (BRBbolus: r=-0.55, BRBslope: r=-0.69, P<0.005) and the SBP responses to phenylephrine during ganglionic blockade (BRBbolus: r=0.53; BRBslope: r=0.98, P<0.0001). BRBbolus was also inversely related to the SBP response to phenylephrine before ganglionic blockade (r=-0.78, P<0.0001). CONCLUSIONS: Physiological aging in men is associated with a marked reduction in baroreflex buffering. The decrease in baroreflex buffering with aging is related to increases in basal sympathetic nerve activity and reductions in systemic alpha1-adrenergic vascular responsiveness. These findings are helpful for interpreting changes in baroreflex buffering in older patients with cardiovascular disease, as well as changes in responsiveness to vasoactive drugs with aging.

Adult↗
PubMed1999

Baroreflex gain predicts blood pressure recovery during simulated ventricular tachycardia in humans.

BACKGROUND: Despite similar degrees of left ventricular dysfunction and similar tachycardia or pacing rate, blood pressure (BP) response and symptoms vary greatly among patients. Sympathetic nerve activity (SNA) increases during sustained ventricular tachycardia (VT), and the magnitude of this sympathoexcitatory response appears to contribute to the net hemodynamic outcome. We hypothesize that the magnitude of sympathoexcitation and thus arterial baroreflex gain is an important determinant of the hemodynamic outcome of VT. METHODS AND RESULTS: We evaluated the relation between arterial baroreflex sympathetic gain and BP recovery during rapid ventricular pacing (VP) in patients referred for electrophysiological study. Efferent postganglionic muscle SNA, BP, and central venous pressure (CVP) were measured in 14 patients during nitroprusside infusion and during VP at 150 (n=12) or 120 (n=2) bpm. Arterial baroreflex gain was defined as the slope of the relationship of change in SNA to change in diastolic BP during nitroprusside infusion. Recovery of mean arterial pressure (MAP) during VP was measured as the increase in MAP from the nadir at the onset of pacing to the steady-state value during sustained VP. Arterial baroreflex gain correlated positively with recovery of MAP (r=0.57, P=0.034). No significant correlation between ejection fraction and baroreflex gain (r=0.48, P=0.08) or BP recovery (r=0.41, P=0.15) was found. When patients were separated into high versus low baroreflex gain, the recovery of MAP during simulated VT was significantly greater in patients with high gain. CONCLUSIONS: These data strongly suggest that arterial baroreflex gain contributes significantly to hemodynamic stability during simulated VT. Knowledge of baroreflex gain in individual patients may help the clinician tailor therapy directed toward sustained VT.

Adult↗
PubMed1996

Reflex control of sympathetic activity during ventricular tachycardia in dogs: primary role of arterial baroreflexes.

BACKGROUND: The determinants of hemodynamic outcome during ventricular tachycardia (VT) are not well understood. In the present study, we addressed the relative contributions of arterial and cardiopulmonary baroreflexes to the sympathetic and arterial pressure responses to VT or ventricular pacing (VP) in dogs with inducible VT. METHODS AND RESULTS: Responses of renal sympathetic nerve activity (RSNA), pulmonary capillary wedge pressure (PCWP), and mean arterial pressure (MAP) to induced VT or VP (220 to 280 beats per minute) were determined in 12 dogs with a healed anteroapical infarction and inducible VT and in 8 control dogs. The responses were determined with all reflexes intact, after selective denervation of either arterial or cardiopulmonary baroreflexes, and after combined denervation. Differences between intact and denervated conditions were used to assess the relative effects of each baroreflex. In the infarct group, responses during VT were comparable to those during VP. RSNA and PCWP increased significantly (P<.01), whereas MAP decreased significantly (P<.001) during VT or VP with baroreflexes intact in both groups. The increase in RSNA and the recovery of MAP during sustained VP were greater in the infarct group (P<.05); in addition, the increase in PCWP was greater in the infarct group (P<.05). Arterial baroreflex denervation abolished the increased RSNA and recovery of MAP during VP in both groups. After cardiopulmonary baroreflex denervation, the increase in RSNA was augmented in both groups (control group more than infarct group), but recovery of MAP was increased further only in the control group. CONCLUSIONS: These results suggest that arterial baroreflex mediated sympathoexcitation plays an important role in determining the hemodynamic outcome during VT, whereas cardiopulmonary baroreflexes play only a modest modulatory role.

Animals↗
PubMed2003

Baroreflex buffering in sedentary and endurance exercise-trained healthy men.

Baroreflex buffering plays an important role in arterial blood pressure control. Previous reports suggest that baroreflex sensitivity may be altered in endurance exercise-trained compared with untrained subjects. It is unknown, however, if in vivo baroreflex buffering is altered in the endurance exercise-trained state in humans. Baroreflex buffering was determined in 36 healthy normotensive men (18 endurance exercise-trained, 41+/-5 [SEM] years; 18 untrained, 41+/-4 years) by measuring the potentiation of the systolic blood pressure responses to a phenylephrine bolus and to incremental phenylephrine infusion during compared with before ganglionic blockade with trimethaphan. The exercise-trained men had a lower resting heart rate and higher maximal oxygen consumption and heart rate variability than the sedentary control subjects (all P=0.01). Mean levels and variability of blood pressure, cardiovagal baroreflex sensitivity (change in heart rate/change in systolic blood pressure), and basal muscle sympathetic nerve activity were not different in the two groups. The systolic blood pressure responses to phenylephrine were not different in the endurance-trained and untrained men before or during ganglionic blockade (P>0.6). Measures of baroreflex buffering with the use of a phenylephrine bolus (3.9+/-0.8 versus 4.0+/-0.7, trained versus untrained, P=0.85) and incremental infusion (2.8+/-0.4 versus 2.5+/-0.6, P=0.67) were similar in the two groups. Baroreflex buffering does not differ in endurance exercise-trained compared with untrained healthy men. These results support the concept that habitual vigorous endurance exercise does not modulate in vivo baroreflex buffering in healthy humans.

Adrenergic alpha-Agonists↗
PubMed2003

Baroreflex control of muscle sympathetic nerve activity after carotid body tumor resection.

Bilateral carotid body tumor resection causes a permanent attenuation of vagal baroreflex sensitivity. We retrospectively examined the effects of bilateral carotid body tumor resection on the baroreflex control of sympathetic nerve traffic. Muscle sympathetic nerve activity was recorded in 5 patients after bilateral carotid body tumor resection (1 man and 4 women, 51+/-11 years) and 6 healthy control subjects (2 men and 4 women, 50+/-7 years). Baroreflex sensitivity was calculated from changes in R-R interval and muscle sympathetic nerve activity in response to bolus injections of phenylephrine and nitroprusside. In addition, sympathetic responses to the Valsalva maneuver and cold pressor test were measured. The integrated neurogram of patients and control subjects contained a similar pattern of pulse synchronous burst of nerve activity. Baroreflex control of both heart rate and sympathetic nerve activity were attenuated in patients as compared with control subjects [heart rate baroreflex sensitivity: 3.68+/-0.93 versus 11.61+/-4.72 ms/mm Hg (phenylephrine, P=0.011) and 2.53+/-1.36 versus 5.82+/-1.94 ms/mm Hg (nitroprusside, P=0.05); sympathetic baroreflex sensitivity: 3.70+/-2.90 versus 7.53+/-4.12 activity/100 beats/mm Hg (phenylephrine, P=0.10) and 3.93+/-4.43 versus 15.27+/-10.03 activity/100 beats/mm Hg (nitroprusside, P=0.028)]. The Valsalva maneuver elicited normal reflex changes in muscle sympathetic nerve activity, whereas heart rate responses were blunted in the patients with bilateral carotid body tumor resection. Maximal sympathetic responses to the cold pressor test did not differ between the two groups. Denervation of carotid sinus baroreceptors as the result of bilateral carotid body tumor resection produces chronic impairment of baroreflex control of both heart rate and sympathetic nerve activity. During the Valsalva maneuver, loss of carotid baroreflex control of heart rate is less well compensated for by the extra carotid baroreceptors than the control of muscle sympathetic nerve activity.

Adult↗
PubMed2005

Selective sensitization by nitric oxide of sympathetic baroreflex in rostral ventrolateral medulla of conscious rabbits.

Nitric oxide (NO) deficiency in the rostral ventrolateral medulla (RVLM) has been implicated in impaired baroreflex control in hypertensive and heart failure animals. However, the role of local NO in normal baroreflex regulation remains unclear. This study aimed to examine the role of NO in tonic and baroreflex control of blood pressure (BP) in the RVLM of conscious rabbits. Microinjections of NO donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside (5 to 20 nmol), or NO itself (20 to 200 pmol) into the RVLM dose-dependently increased BP. Bilateral microinjections of an NO synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 10 nmol), its inactive enantiomer D-NAME, or soluble guanylate cyclase (sGC) inhibitors, 1-H-[1,2,4]oxadiaolo[4,3-a]quinoxalin-1-one (ODQ, 250 pmol) and methylene blue (10 nmol), into the RVLM did not affect resting BP, heart rate, or renal sympathetic nerve activity (RSNA). However, L-NAME, methylene blue, and ODQ decreased RSNA baroreflex gain by 42% to 55%, whereas D-NAME did not affect this reflex. Co-microinjections of L-NAME and superoxide scavenger tempol (20 nmol) decreased RSNA baroreflex gain by 37+/-8%. Microinjections of a neuronal NOS (nNOS) inhibitor, 7-nitroindazole (500 pmol), into the RVLM decreased RSNA baroreflex gain by 42+/-12%, without altering resting BP, heart rate, or RSNA. Local administration of inducible NOS (iNOS) inhibitors, S-methylisothiourea (0.25 nmol) and aminoguanidine (0.25 and 2.5 nmol), affected neither resting nor baroreflex parameters. These results suggest that nNOS-derived NO facilitates sympathetic baroreflex transmission in the RVLM at least in part via a sGC-dependent, superoxide-independent mechanism. However, local nNOS and iNOS play little role in the tonic support of BP in conscious rabbits.

Animals↗
PubMed2005

Slow breathing improves arterial baroreflex sensitivity and decreases blood pressure in essential hypertension.

Sympathetic hyperactivity and parasympathetic withdrawal may cause and sustain hypertension. This autonomic imbalance is in turn related to a reduced or reset arterial baroreflex sensitivity and chemoreflex-induced hyperventilation. Slow breathing at 6 breaths/min increases baroreflex sensitivity and reduces sympathetic activity and chemoreflex activation, suggesting a potentially beneficial effect in hypertension. We tested whether slow breathing was capable of modifying blood pressure in hypertensive and control subjects and improving baroreflex sensitivity. Continuous noninvasive blood pressure, RR interval, respiration, and end-tidal CO2 (CO2-et) were monitored in 20 subjects with essential hypertension (56.4+/-1.9 years) and in 26 controls (52.3+/-1.4 years) in sitting position during spontaneous breathing and controlled breathing at slower (6/min) and faster (15/min) breathing rate. Baroreflex sensitivity was measured by autoregressive spectral analysis and "alpha angle" method. Slow breathing decreased systolic and diastolic pressures in hypertensive subjects (from 149.7+/-3.7 to 141.1+/-4 mm Hg, P<0.05; and from 82.7+/-3 to 77.8+/-3.7 mm Hg, P<0.01, respectively). Controlled breathing (15/min) decreased systolic (to 142.8+/-3.9 mm Hg; P<0.05) but not diastolic blood pressure and decreased RR interval (P<0.05) without altering the baroreflex. Similar findings were seen in controls for RR interval. Slow breathing increased baroreflex sensitivity in hypertensives (from 5.8+/-0.7 to 10.3+/-2.0 ms/mm Hg; P<0.01) and controls (from 10.9+/-1.0 to 16.0+/-1.5 ms/mm Hg; P<0.001) without inducing hyperventilation. During spontaneous breathing, hypertensive subjects showed lower CO2 and faster breathing rate, suggesting hyperventilation and reduced baroreflex sensitivity (P<0.001 versus controls). Slow breathing reduces blood pressure and enhances baroreflex sensitivity in hypertensive patients. These effects appear potentially beneficial in the management of hypertension.

Arteries↗
PubMed2006

Renal denervation does not abolish sustained baroreflex-mediated reductions in arterial pressure.

Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean arterial pressure and plasma norepinephrine concentration were 95+/-2 mm Hg and 96+/-12 pg/mL, respectively. During day 1 of baroreflex activation, mean arterial pressure decreased 13+/-1 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean arterial pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with sustained decreases in plasma norepinephrine concentration ( approximately 50%) and plasma renin activity (30% to 40%). All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean arterial pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were comparable to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were similar to those observed before renal denervation. These findings demonstrate that the presence of the renal nerves is not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex.

Animals↗
PubMed1996

Noninvasive assessment of baroreflex control in borderline hypertension. Comparison with the phenylephrine method.

In this study, we examined the sensitivity of two recently developed noninvasive baroreflex measurement techniques to assess baroreflex control in hypertension. We assessed baroreflex sensitivity noninvasively from covariations of systolic pressure and RR interval using spectral analysis and sequence detection. The noninvasive estimates of baroreflex control were compared with estimates derived from phenylephrine-induced increases in systolic pressure and RR interval in normotensive subjects (n = 27) and borderline hypertensive subjects (n = 15). Baroreflex sensitivity was significantly reduced in the borderline hypertensive group relative to the normotensive group when assessed with the use of either the noninvasive or invasive methods to index baroreflex control. In addition, estimates obtained from the noninvasive methods were significantly correlated with baroreflex sensitivity assessed with the phenylephrine method (spectral: r = .48, P < .001; sequence: r = .50, P < .001). These findings suggest that spectral analysis and the sequence method provide viable alternatives to the pharmacological approach for estimation of baroreflex sensitivity in hypertension.

Adult↗
PubMed1997

Angiotensin II blockade [corrected] enhances baroreflex control of sympathetic outflow in heart failure.

Enhanced sympathetic outflow is seen in both patients with congestive heart failure and animals with experimental heart failure. In a previous study, we demonstrated that the baroreflex control of heart rate was impaired in conscious rabbits with pacing-induced heart failure and that this impairment was partially restored by blockade of angiotensin II type 1 (AT1) receptors. In the present study, we determined the interaction between the renin-angiotensin system and baroreflex control of renal sympathetic nerve activity in normal conscious rabbits and conscious rabbits with pacing-induced heart failure before and after AT1 receptor blockade. Heart failure was induced by rapid ventricular pacing at a rate of 360 to 380 beats per minute for an average of 16.7 +/- 0.6 days. To generate baroreflex curves, we altered arterial pressure by administering phenylephrine and sodium nitroprusside. A sigmoidal logistic function was fit to renal sympathetic nerve activity-mean arterial pressure relationships for analysis of several components of baroreflex function. AT1 receptors were blocked by intravenous administration of the specific antagonist L-158,809. In normal rabbits, there was no significant difference in any parameter of baroreflex function before and after blockade of AT1 receptors. In contrast, blockade of AT1 receptors enhanced baroreflex sensitivity in heart failure rabbits. The maximal gain increased to 5.0 +/- 0.7% renal sympathetic nerve activity/mm Hg from 2.6 +/- 0.3 (P < .05). Although L-158,809 had no effect on baseline renal sympathetic nerve activity in normal rabbits, analysis of the data in the heart failure rabbits indicated that baseline renal sympathetic nerve activity was reduced from 33 +/- 5% to 17 +/- 4% after L-158,809 administration after adjustment for changes in arterial pressure. These data suggest that angiotensin II plays a role in baroreflex impairment in this model of heart failure and may be in part responsible for the depressed baroreflex sensitivity observed in heart failure.

Angiotensin II↗
PubMed2001

Baroreflex sensitivity and oxidative stress in adriamycin-induced heart failure.

Adriamycin cardiotoxicity is associated with oxidative stress in the presence of globally depressed cardiac function. It is unknown if there is a similar profile with early diastolic changes and how it relates to baroreflex control of circulation. In this study, we evaluated baroreflex control of circulation in adriamycin-treated Wistar rats compared with controls, using invasive blood pressure recording processed by a data acquisition system (CODAS, 1 KHz). Baroreflex sensitivity was evaluated by modulating blood pressure with phenylephrine and sodium nitroprusside. Oxidative stress was quantified by chemiluminescence and by glutathione peroxidase enzyme activity. Diastolic dysfunction was characterized by increased left ventricle end-diastolic pressure in adriamycin-treated rats compared with controls with preserved ascending aortic flow. Baroreflex sensitivity in response to blood pressure elevation and reduction were similar in adriamycin (-2+/-0.27 and -3.19+/-0.56 bpm/mm Hg) and control rats (-1.35+/-0.15 and -2.52+/-0.39 bpm/mm Hg). Chemiluminescence was higher (20450+/-1286 versus 16517+/-1020 counts per second/mg protein) and glutathione peroxidase activity was lower (45.6+/-4.3 versus 76.4+/-6.9 micromol. min(-1). mg(-1) protein) in adriamycin rats compared with controls. Inverse correlations were observed between glutathione peroxidase activity and left ventricle end-diastolic pressure (r=-0.72, P=0.02), between baroreflex sensitivity to phenylephrine and left ventricle end-diastolic pressure (r=-0.77, P=0.004), and between chemiluminescence and baroreflex sensitivity to sodium nitroprusside (r=-0.75, P=0.02), whereas a positive correlation was observed between baroreflex sensitivity to sodium nitroprusside and glutathione peroxidase activity (r=0.7, P=0.04). Thus, adriamycin led to increased left ventricle end-diastolic pressure without changes in baroreflex sensitivity, and associated increased oxidative stress appeared to be related to reduction of reflex control of circulation.

Analysis of Variance↗
PubMed2006

Orchiectomy or androgen receptor blockade attenuates baroreflex-mediated bradycardia in conscious rats.

BACKGROUND: Previous studies have shown that testosterone enhances baroreflex bradycardia. Therefore, conscious unrestrained rats were used to investigate the role of the androgen receptor in the testosterone-mediated modulation of baroreflex bradycardia. Androgen depletion (3 weeks), and androgen receptor blockade (20-24 h), were implemented to test the hypothesis that testosterone influences baroreflex bradycardia via its activity at the androgen receptor in male rats. Phenylephrine (1-16 microg kg(-1)) was used to assess baroreflex bradycardia. RESULTS: Androgen depletion attenuated baroreflex bradycardia (P < 0.01). The antiandrogen flutamide (5, 15, or 30 mg kg(-1), s.c.) caused dose-related attenuation of baroreflex bradycardia in spite of a significant (P < 0.05) increase in serum testosterone. The latter did not lead to increased serum 17beta-estradiol level. CONCLUSION: The data suggest: 1) Androgen depletion or adequate androgen receptor blockade attenuates baroreflex bradycardia. 2) The reflex increase in serum testosterone may counterbalance the action of the lower doses (5 or 15 mg kg(-1)) of flutamide. 3) The absence of a change in serum 17beta-estradiol rules out its contribution to flutamide action on baroreflex bradycardia.

Androgen Antagonists↗
PubMed2003

Effects of repeated Valsalva maneuver straining on cardiac and vasoconstrictive baroreflex responses.

INTRODUCTION: We hypothesized that repeated respiratory straining maneuvers (repeated SM) designed to elevate arterial BPs (arterial baroreceptor loading) would acutely increase baroreflex responses. METHODS: We tested this hypothesis by measuring cardiac baroreflex responses to carotid baroreceptor stimulation (neck pressures), and changes in heart rate and diastolic BP after reductions in BP induced by a 15-s Valsalva maneuver in 10 female and 10 male subjects at 1, 3, 6, and 24 h after performing repeated SM. Baroreflex responses were also measured in each subject at 1, 3, 6, and 24 h at the same time on a separate day without repeated SM (control) in a randomized, counter-balanced cross-over experimental design. RESULTS: There was no statistical difference in carotid-cardiac and peripheral vascular baroreflex responses measured across time following repeated SM compared with the control condition. Integrated cardiac baroreflex response (deltaHR/ deltaSBP) measured during performance of a Valsalva maneuver was increased by approximately 50% to 1.1 +/- 0.2 bpm x mm Hg(-1) at 1 h and 1.0 +/- 0.1 bpm x mm Hg(-1) at 3 h following repeated SM compared with the control condition (0.7 +/- 0.1 bpm x mm Hg(-1) at both 1 and 3 h, respectively). However, integrated cardiac baroreflex response after repeated SM returned to control levels at 6 and 24 h after training. These responses did not differ between men and women. CONCLUSIONS: Our results are consistent with the notion that arterial baroreceptor loading induced by repeated SM increased aortic, but not carotid, cardiac baroreflex responses for as long as 3 h after repeated SM. We conclude that repeated SM increases cardiac baroreflex responsiveness which may provide patients, astronauts, and high-performance aircraft pilots with protection from development of orthostatic hypotension.

Adult↗
PubMed1998

Active standing and passive tilting similarly reduce the slope of spontaneous baroreflex in healthy subjects.

Non-invasive assessment of the sensitivity of cardiac baroreflex was performed by recording each RR-interval and each blood pressure cycle (Finapres). In sequences of at least three cardiac cycles in which systolic blood pressure and RR-interval had changed in the same direction, the slope of linear regression of RR duration as a function of the change in systolic arterial pressure was taken for estimating the sensitivity of the spontaneous cardiac baroreflex. This technique was used in healthy humans to examine how a postural change from supine to upright by either active standing up or 60 degrees head-up tilting modified the sensitivity of the spontaneous baroreflex. We observed that the slope of the spontaneous baroreflex averaged 14.6 +/- 2 ms.mm Hg-1 during rest in the supine position, and decreased to 7.8 +/- 1.2 ms.mm Hg-1 (p < 0.05) after active standing, while the number of sequences was significantly increased in the upright as compared to the supine position. Head-up tilting by 60 degrees led to values similar to those following active standing. The adjustment of baroreflex slope to either postural change occurred in a few seconds, so that posture-characteristic values were obtained from five-minute records. We conclude that non-invasive recording of spontaneous sequences of related changes in blood pressure and RR-interval during several minutes provides reproducible values of the slope of cardiac baroreflex in the supine and upright position. This easy and reliable determination of the sensitivity of the cardiac baroreflex might prove to be useful when assessment of baroreflex function is needed.

Adult↗
PubMed1991

Baroreflex function in normal pregnancy.

The sinoaortic baroreflex is one of the primary mechanisms that regulates blood pressure. Decreased baroreflex sensitivity has been reported in preeclampsia. We sought to determine whether pregnancy altered baroreflex sensitivity. From a radial artery catheter, heart rate and mean arterial pressure were recorded continuously onto a polygraph. The ratio of change in heart rate produced per unit of change in mean arterial pressure was calculated as an index of baroreflex sensitivity. Mean arterial pressure responses to incremental infusions of phenylephrine (0.4 to 2.0 micrograms/kg/min) were measured in the same patients at term (n = 9, 38.0 +/- 0.3 weeks) and again 6 to 8 weeks postpartum (n = 7). The results indicated (1) higher baroreflex sensitivity in pregnancy than in the postpartum period (0.9 vs 0.5 beats/min/mm Hg) (p less than 0.007); (2) attenuated vascular responsiveness to alpha-adrenergic stimulation in pregnancy (p less than 0.05); (3) a relationship between vascular responsiveness and baroreflex sensitivity. We conclude that pregnancy is associated with an increase in baroreflex sensitivity and that the attenuated response to phenylephrine is, at least in part, a result of increased baroreflex sensitivity.

Adolescent↗