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PubMed1997

Effects of aerobic exercise training and yoga on the baroreflex in healthy elderly persons.

It is unclear whether the age-associated reduction in baroreflex sensitivity is modifiable by exercise training. The effects of aerobic exercise training and yoga, a non-aerobic control intervention, on the baroreflex of elderly persons was determined. Baroreflex sensitivity was quantified by the alpha-index, at high frequency (HF; 0.15-0.35 Hz, reflecting parasympathetic activity) and mid-frequency (MF; 0.05-0.15 Hz, reflecting sympathetic activity as well), derived from spectral and cross-spectral analysis of spontaneous fluctuations in heart rate and blood pressure. Twenty-six (10 women) sedentary, healthy, normotensive elderly (mean 68 years, range 62-81 years) subjects were studied. Fourteen (4 women) of the sedentary elderly subjects completed 6 weeks of aerobic training, while the other 12 (6 women) subjects completed 6 weeks of yoga. Heart rate decreased following yoga (69 +/- 8 vs. 61 +/- 7 min-1, P < 0.05) but not aerobic training (66 +/- 8 vs. 63 +/- 9 min-1, P = 0.29). VO2 max increased by 11% following yoga (P < 0.01) and by 24% following aerobic training (P < 0.01). No significant change in alpha MF (6.5 +/- 3.5 vs. 6.2 +/- 3.0 ms mmHg-1, P = 0.69) or alpha HF (8.5 +/- 4.7 vs. 8.9 +/- 3.5 ms mmHg-1, P = 0.65) occurred after aerobic training. Following yoga, alpha HF (8.0 +/- 3.6 vs. 11.5 +/- 5.2 ms mmHg-1, P < 0.01) but not alpha MF (6.5 +/- 3.0 vs. 7.6 +/- 2.8 ms mmHg-1, P = 0.29) increased. Short-duration aerobic training does not modify the alpha-index at alpha MF or alpha HF in healthy normotensive elderly subjects. alpha HF but not alpha MF increased following yoga, suggesting that these parameters are measuring distinct aspects of the baroreflex that are separately modifiable.

Aged↗
PubMedDate not supplied

Angiotensin II modulation of the arterial baroreflex: role of the area postrema.

1. Resetting the operating point of the arterial baroreflex appears to be an important factor involved in determining the level of sympathetic outflow. 2. Substantial data indicate that circulating angiotensin (Ang)II can reset the arterial baroreflex to higher operating pressures. 3. This action of AngII to increase the level of sympathetic nervous system outflow relative to blood pressure may contribute to elevated mean arterial pressure (MAP) during AngII hypertension, as well as to the maintenance of MAP during low sodium states. 4. In most instances, the resetting observed during elevated peripheral AngII is dependent on the area postrema (AP). 5. Although the central mechanisms by which the arterial baroreflex resets to different operating pressures remain to be completely defined, the AP may provide a separate mechanism whereby humoral factors can modulate the operating point of the arterial baroreflex.

Adrenergic Fibers↗
PubMed2002

Tight mechanism correlation between heart rate turbulence and baroreflex sensitivity: sequential autonomic blockade analysis.

INTRODUCTION: Heart rate turbulence is a powerful de novo risk predictor for patients surviving acute myocardial infarction. However, little is known about its underlying physiologic mechanism. METHODS AND RESULTS: Hypothesizing that heart rate turbulence is barorceptor reflex related, we studied heart rate and blood pressure fluctuations at rest and after systematically introduced ventricular premature beats in 16 patients without structural heart disease (10 men and 6 women; mean age 45 +/- 17 years) before and after sequential sympathetic (esmolol 4-mg bolus followed by 120 microg/kg/min intravenously), parasympathetic (atropine 0.04 mg/kg intravenously), and combined autonomic blockade (esmolol plus atropine). Turbulence onset (%) and turbulence slope (msec/beat) were averaged from 10 respective ventricular premature beats. Spontaneous baroreflex sensitivity (msec/mmHg) was calculated from 5 minutes of sinus rhythm recording. The results showed that turbulence slope decreased after atropine (0.71 +/- 0.50 msec/beat vs 5.17 +/- 3.96 msec/beat at baseline; P < 0.01) and combined autonomic blockade (1.23 +/- 1.02 msec/beat; P < 0.01) but was unchanged after esmolol (4.53 +/- 3.30 msec/beat; P > 0.05). Turbulence onset increased after atropine (0.32% +/- 0.35% vs -0.45 +/- 0.94 at baseline; P < 0.05) and combined sympathetic and parasympathetic blockade (0.58% +/- 0.86%; P < 0.05) but was unchanged after esmolol (-0.62% +/- 1.33%; P > 0.05). Turbulence slope was positively correlated with baroreflex sensitivity at baseline (r = 0.78, P < 0.01) and after esmolol (r = 0.8, P < 0.01), but dissociated after atropine (r = 0.16, P > 0.05) and combined autonomic blockade (r = 0.31, P > 0.05). Turbulence onset was negatively correlated with baroreflex sensitivity at baseline (r = -0.61, P < 0.05), after esmolol (r = -0.80, P < 0.01), and after atropine (r = -0.53, P < 0.05). CONCLUSION: Heart rate turbulence of turbulence onset and turbulence slope is critically vagal dependent and highly correlated with spontaneous baroreflex sensitivity, which underscores its clinical importance in cardiovascular risk stratification.

Adult↗
PubMed2001

Role of angiotensin II in altered baroreflex function of conscious rabbits during late pregnancy.

OBJECTIVE: Pregnancy alters baroreflex control of heart rate in conscious rabbits, but the mechanism for this action is unknown. This study tested the hypothesis that endogenous angiotensin II is the mediator. STUDY DESIGN: To test this hypothesis the baroreflex relationship between arterial pressure and heart rate in conscious rabbits was determined before and after administration of the angiotensin II AT1 receptor antagonist losartan (n = 7) before pregnancy and at the end of gestation. RESULTS: Pregnancy decreased mean arterial pressure, increased heart rate, and modified the reflex by shifting the mean arterial pressure-heart rate relationship to a lower pressure level, by increasing minimum heart rate, and by decreasing baroreflex gain (P < .05). Before pregnancy, losartan decreased baroreflex gain but had no other effect on reflex function. In contrast, during late gestation losartan further decreased mean arterial pressure, further decreased reflex gain, decreased maximum heart rate, and shifted the curve to a lower mean arterial pressure level (P < .05). CONCLUSION: These results suggest that in conscious rabbits during pregnancy endogenous angiotensin II contributes to hypotension-induced tachycardia but does not decrease reflex gain or elevate minimum heart rate.

Angiotensin II↗
PubMed2001

Reduced baroreflex sensitivity and blunted endogenous nitric oxide synthesis precede the development of hypertension in TGR(mREN2)27 rats.

Transgenic TGR(mREN2)27 (TGR) rats are an animal model of fulminant hypertension characterized by an inverse circadian blood pressure profile. The present study addressed the contribution of nitric oxide (NO) synthesis and baroreflex function to hypertension and the inverse blood pressure pattern. NO synthesis was measured at four different times of day indirectly by excretion of NO metabolites (NOx: NO2- and NO3-) in the urine of 5- and 11-week-old TGR and Sprague-Dawley (SPRD) controls. Blood pressure, heart rate, and motor activity were recorded in age-matched rats of both strains using an implantable telemetry system. Beat-to-beat recording of blood pressure and pulse interval was performed hourly in 6-week-old animals over 24 h. From these data, baroreflex sensitivity (BRS) was calculated by linear regression of spontaneous fluctuations of blood pressure and corresponding changes of pulse interval. Baroreflex sensitivity was lower in pre-hypertensive TGR rats than in SPRD rats, and the reduction was restricted to the daily resting period. In both strains, NOx excretion showed circadian rhythmicity, with peak values during the activity period at night. Interestingly, excretion of NOx was reduced during the resting period in 5-week-old TGR rats prior to the development of hypertension. Impairment of NO synthesis and baroreflex function precede the development of hypertension in TGR rats. The reduction of both parameters was restricted to the resting period and, therefore, could be involved in the development of the inverse circadian blood pressure profile of TGR rats.

Animals↗
PubMed2000

Post-exercise elevations in sympathetic nerve activity and baroreflex function in normotensive rabbits.

We tested the hypothesis that a single bout of dynamic exercise reduces post-exercise arterial pressure, heart rate, and renal sympathetic nerve activity and attenuates the arterial baroreflex control of heart rate and renal sympathetic nerve activity in normotensive New Zealand White rabbits. Animals were chronically instrumented with right jugular venous and left femoral arterial catheters, and electrodes around the renal sympathetic nerve. Arterial pressure, heart rate, and renal sympathetic nerve activity were recorded for two hours pre-exercise and two hours after a single bout of treadmill exercise (post-exercise). Post-exercise heart rate, arterial pressure, and renal sympathetic nerve activity were elevated above pre-exercise values (71+/-3 bpm, 13+/-1 mmHg, and 80+/-21%, respectively). These data demonstrate that normotensive rabbits do not exhibit post-exercise hypotension, due in part to elevations in sympathetic nerve activity. In addition, arterial baroreflex regulation of heart rate and renal sympathetic nerve activity were determined pre- and post-exercise. Exercise shifted the baroreflex function curve for heart rate and renal sympathetic nerve activity upward and to the right without a change in gain. These data suggest that post-exercise elevations in sympathetic nerve activity are due, in part, to an elevation of the operating point of the arterial baroreflex to a higher pressure. These responses in normotensive rabbits contrast sharply with the responses in hypertensive individuals and animals. Understanding the mechanisms contributing to the differences between hypertensive and normotensive subjects may lead to measures designed to lower arterial pressure in hypertensive individuals.

Animals↗
PubMed1997

Baroreflex function in sedentary and endurance-trained elderly people.

OBJECTIVE: to determine the differences associated with age and endurance exercise training on the baroreflex function of healthy subjects. DESIGN: cross-sectional study. SETTING: university research department. PARTICIPANTS: 26 (10 female) sedentary, healthy, normotensive elderly subjects (mean age 67 years, range 62-81), eight (two female) elderly endurance-trained athletes (66 years, 62-69) and eight (two female) young (30 years, 25-34) subjects. MEASUREMENTS: baroreflex sensitivity was quantified by the alpha-index, at high frequency (HF, 0.15-0.35 Hz) and mid frequency (MF, 0.05-0.15 Hz), derived from spectral and cross-spectral analysis of spontaneous fluctuations in heart rate and blood pressure. RESULTS: resting heart rate was significantly lower in endurance-trained athletes than sedentary elderly people (58 +/- 12 versus 68 +/- 11 min(-1), P < 0.05) but not different to that in healthy young subjects (63 +/- 9 min[-1]). alpha(HF) in sedentary elderly subjects (8.1 +/- 4.2 ms.mm Hg[-1]) was lower than both endurance-trained elderly athletes (14.8 +/- 4.8 ms.mm Hg(-1), P < 0.05) and healthy young subjects (28.3 +/- 21.8 ms.mm Hg(-1), P < 0.05) and was not significantly different between endurance-trained elderly athletes and healthy young subjects (P = 0.10). alpha(MF) in healthy young subjects (15.4 +/- 8.8 ms.mm Hg[-1]) was greater than in sedentary elderly subjects (6.5 +/- 3.2 ms.mm Hg(-1), P < 0.01) and endurance-trained elderly athletes (6.9 +/- 2.0 ms.mmHg(-1), P < 0.01), while there was no significant difference between the two elderly groups (P = 0.66). CONCLUSIONS: both components of the baroreflex measured by the alpha-index show a decrease with age. Elderly endurance-trained athletes have less reduction in the high, but not mid, frequency component of the alpha-index compared with sedentary elderly subjects. Some of the age-related changes in baroreflex sensitivity may be related to physical fitness and activity levels.

Adult↗
PubMed2002

Genetic and pharmacological dissection of pathways involved in the angiotensin II-mediated depression of baroreflex function.

Heart failure and hypertension are associated with increases in angiotensin II (ANG II) activity. One brain area where ANG II effects may be particularly important in these situations is the nucleus of the solitary tract (NTS). Located in the dorsomedial medulla, the NTS is the termination site of baroreceptor afferents and is essential for mediating the baroreflex. In hypertensive animals the baroreflex is impaired; this may be reversed by antagonizing ANG II AT1 receptors in the NTS. Recently, we showed that the baroreflex depressant action of ANG II in the NTS is mediated by activation of endothelial nitric oxide synthase (eNOS) and enhanced release of GABA. Using conventional pharmacological tools and a range of adenoviral-mediated expression of dominant negative proteins, we have determined the intracellular pathway(s) in the NTS by which ANG II activates eNOS. Our data indicate that ANG II acting in the NTS depresses the baroreflex via a Gq protein-mediated activation of phospholipase C, which through 1,4,5-inositol triphosphate causes release of calcium from the IP3-sensitive intracellular stores and calcium-calmodulin formation. In contrast, multiple site disruption of a pathway leading to eNOS activation via the serine/threonine kinase Akt was ineffective

Angiotensin II↗
PubMed1995

A comparison of baroreflex sensitivity during isoflurane and desflurane anesthesia in humans.

BACKGROUND: Desflurane anesthesia has been associated with heart rate (HR) and sympathetic nerve activity (SNA) responses that differ from those during isoflurane anesthesia. Whether these differences might be due to better preservation by desflurane of the baroreceptor reflex control of HR or SNA in humans was examined. METHODS: Baroreflex sensitivity was assessed in 18 volunteers anesthetized with either desflurane or isoflurane. Measurements of HR, blood pressure (BP), and efferent SNA (percutaneous recordings from the peroneal nerve) were made, and baroreflex sensitivity was evaluated at conscious baseline and during 0.5, 1.0, and 1.5 MAC anesthesia. Baroreflex responses were triggered by bolus intravenous injections of nitroprusside (100 micrograms) and phenylephrine (150 micrograms). The linear portions of the baroreflex curves relating HR to mean arterial pressure and relating SNA to diastolic pressure were determined to obtain cardiac and sympathetic baroslopes, respectively. RESULTS: Cardiac (HR) baroslopes were equally diminished at increasing MAC of both anesthetics. Sympathetic baroslopes were preserved at 0.5 MAC isoflurane but diminished at 0.5 MAC desflurane. Higher MAC produced equal depression of sympathetic baroslopes with both anesthetics. CONCLUSIONS: Increasing MAC of desflurane and isoflurane anesthesia results in similar and progressive decreases in BP but dissimilar SNA and HR responses. These differences are not explained by disparate effects of these anesthetics on the baroreceptor reflex control of SNA or HR.

Adult↗
PubMed2001

Moderate hypothermia depresses arterial baroreflex control of heart rate during, and delays its recovery after, general anesthesia in humans.

BACKGROUND: Effects of hypothermia on arterial baroreflex function during, and on its recovery after, general anesthesia were examined in humans. METHODS: Twenty healthy volunteers were randomly assigned to a normothermic group (n = 10 each, active forced-air warming) or to a hypothermic group (no active warming) during anesthesia. Measurements of R-R intervals and systolic blood pressure were made at conscious baseline and at 20, 60, and 120 min after the induction and 20, 60, 120, and 180 min after emergence from general anesthesia with sevoflurane for 2 h. Ventilation was mechanically controlled, and end-tidal sevoflurane concentration was maintained at 2% during anesthesia. Baroreflex responses were triggered by bolus intravenous injections of phenylephrine and nitroprusside. The linear portions of the baroreflex curves relating R-R intervals and systolic blood pressure were determined to obtain baroslopes. RESULTS: During anesthesia, the mean lowest tympanic temperature of the hypothermia group (33.9+/-0.5 degrees C [mean +/- SD]) was significantly lower than that of the normothermia group (36.1+/-0.7 degrees C, P < 0.001). The baroslopes of the pressor and depressor tests were decreased by 19-39% during and by 27-53% after general anesthesia in the hypothermia group, compared with the normothermia group (P < 0.05). The baroslopes of the normothermia group returned to the baseline values at 60 min after anesthesia, whereas the pressor test sensitivity of the hypothermia group was significantly less than that of the normothermia group for the entire course of recovery. CONCLUSIONS: The results indicate that moderate hypothermia enhances anesthesia-induced depression of baroreflex function in anesthetized humans and delays its recovery after general anesthesia.

Adult↗
PubMed1995

Baroreflex control of heart rate in Dahl hypertensive (SS/Jr) and normotensive (SR/Jr) rats.

OBJECTIVE: To determine whether impaired reflex control of heart rate was evident in rats of the inbred Dahl hypertension-sensitive (SS/Jr) strains. DESIGN AND METHODS: Phenylephrine and sodium nitroprusside were administered through jugular catheters in graded doses to elicit a range of pressor and depressor responses, for which corresponding reflex decreases and increases in heart rate were recorded. To assess the relative contributions of sympathetic and parasympathetic branches of autonomic control to baroreflex functioning, atropine methyl nitrate and atenolol were administered to establish vagal blockade, and cardiac sympathetic blockade, respectively. RESULTS: Assuming a sigmoidal relationship between mean arterial pressure and heart rate changes, our results indicated that SS/Jr rats exhibited elevated blood pressure set-points for baroreceptor activation and roughly similar baroreflex sensitivity compared with SR/Jr rats. In contrast, using linear regression analyses, our results indicated that SS/Jr rats had significant reductions in baroreceptor sensitivity when arterial pressure was increased by phenylephrine. Baroreceptor sensitivity was similar between rats of the two strains when arterial pressure was reduced by administration of nitroprusside. Atropine and atenolol had similar effects on baroreflex control of heart rate in both strains. However, pressor responses to phenylephrine were significantly greater in SS/Jr rats, an effect which had previously been reported in Dahl salt-sensitive (DS) rats and attributed to deficits in autonomic reflex control of vascular resistance. CONCLUSION: The present results indicate that the method of analysis for determination of baroreceptor sensitivity can influence the conclusions drawn in studies of hypertensive and normotensive strains of rat. Although deficits in baroreflex control of heart rate have consistently been reported in DS rats, the present results did not confirm those findings in inbred Dahl rats when mean arterial pressure and heart rate change data were analyzed by fitting a logistic equation to sigmoid data. In contrast, using linear regression analysis, those same data did reveal a defect in baroreceptor sensitivity of SS/Jr rats after acute increases in arterial pressure. Caution should be exercised in the selection of a method for analysis of baroreceptor data and the interpretation of the findings.

Animals↗
PubMed1998

Effect of chronic angiotensin converting enzyme inhibition on sympathetic nerve traffic and baroreflex control of the circulation in essential hypertension.

BACKGROUND: Human studies have shown that the blood pressure lowering effects of angiotensin converting enzyme inhibitors are accompanied by a reduction in plasma norepinephrine levels. Whether this is due to central or peripheral mechanisms is unknown, however. OBJECTIVE: To evaluate the effects of chronic interference with the renin-angiotensin system on sympathetic nerve traffic and baroreflex control of vagal and adrenergic cardiovascular drive. PATIENTS AND METHODS: In 18 untreated mild to moderate essential hypertensive patients aged 48.5+/-1.9 years (mean+/-SEM), we measured mean arterial pressure (Finapres), heart rate (electrocardiogram), plasma renin activity (radioimmunoassay), plasma norepinephrine (high-performance liquid chromatography) and postganglionic muscle sympathetic nerve activity (microneurography at a peroneal nerve). In nine patients, measurements were performed before and after 2 months of oral administration of lisinopril (10 mg/day), while in the remaining nine patients they were performed before and after a 2 month observation period, without the drug administration. Measurements were performed at rest and during baroreflex stimulation and deactivation elicited by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. RESULTS: Lisinopril induced a marked increase in plasma renin activity (from 1.1+/-0.2 to 6.4+/-1.3 ng/ml per h, P< 0.01) and a reduction in mean arterial pressure (from 109.6+/-3.1 to 98.7+/-2.9 mmHg, P < 0.01) without affecting the heart rate. Plasma norepinephrine and muscle sympathetic nerve activity values were not significantly different before and after lisinopril treatment (plasma norepinephrine values changed from 290.4+/-39.2 to 308.1+/-67.1 pg/ml; muscle sympathetic nerve activity changed from 56.4+/-5.3 to 50.6+/-6.6 bursts/100 heart beats). Neither the sympathoinhibitory nor the sympathoexcitatory responses to phenylephrine and nitroprusside were affected by lisinopril, nor the concomitant bradycardia and tachycardia. The curves relating mean arterial pressure to heart rate and muscle sympathetic nerve activity values during baroreceptor manipulation were shifted to the left, indicating a resetting of the baroreflex to the lower blood pressure values achieved during treatment. CONCLUSIONS In essential hypertension, sympathetic nerve traffic is not affected by chronic angiotensin converting enzyme inhibitor treatment that effectively interferes with the renin-angiotensin system and lowers the elevated blood pressure. The baroreflex ability to modulate heart rate and central sympathetic outflow is also unaffected. These data argue against the existence of a central sympathoexcitatory effect of angiotensin II in this condition. They also indicate that antihypertensive treatment with an angiotensin converting enzyme inhibitor preserves autonomic reflex control, with favorable consequences for cardiovascular homeostasis.

Administration, Oral↗
PubMed2001

Slow breathing reduces chemoreflex response to hypoxia and hypercapnia, and increases baroreflex sensitivity.

OBJECTIVE: To investigate whether breathing more slowly modifies the sensitivity of the chemoreflex and baroreflex. DESIGN SETTING: University of Pavia, IRCCS Policlinico S. Matteo. PARTICIPANTS: Fifteen healthy individuals. INTERVENTIONS: Progressive isocapnic hypoxia and progressive hyperoxic hypercapnia were measured during spontaneous breathing and during a breathing rate fixed at 6 and 15 breaths per minute (b.p.m.). MAIN OUTCOME MEASURES: Variations in chemo- and baroreflex sensitivity (by monitoring ventilation, oxygen saturation, end-tidal carbon dioxide, R-R interval and blood pressure) induced by different breathing rates. RESULTS: Breathing at 6 b.p.m. depressed (P < 0.01) both hypoxic and hypercapnic chemoreflex responses, compared with spontaneous or 15 b.p.m. controlled breathing. Hypoxic and hypercapnic responses during spontaneous breathing correlated with baseline spontaneous breathing rate (r = -0.52 and r = +0.51, respectively; P = 0.05). Baroreflex sensitivity was greater (P < 0.05) during slow breathing at baseline and remained greater at end rebreathing. CONCLUSIONS: Slow breathing reduces the chemoreflex response to both hypoxia and hypercapnia. Enhanced baroreflex sensitivity might be one factor inhibiting the chemoreflex during slow breathing. A slowing breathing rate may be of benefit in conditions such as chronic heart failure that are associated with inappropriate chemoreflex activation.

Adult↗
PubMed1995

Comparison of the effects of angiotensin II, losartan, and enalapril on baroreflex control of heart rate in conscious rabbits.

We compared the effects of angiotensin II (AII), enalapril, and losartan given by acute intravenous (i.v.) injection, on cardiac baroreflex sensitivity in two groups of conscious normotensive rabbits bred for high gain [> 5 beats/min/mm Hg] (group I) and low gain [< 4 beats/min/mm Hg] (group II) of the mean arterial blood pressure-heart rate (MAP/HR) relationship, respectively. Full sigmoid barocurves were produced in 62 rabbits by i.v. injection of phenylephrine (PE 1-15 micrograms/kg) and nitroglycerin (NTG 1-20 micrograms/kg) after pretreatment with saline or with AII, enalapril, or losartan. In group II, AII had a biphasic effect on baroreflex sensitivity; at 10 and 50 ng/kg/min, it increased the gain from 3.47 +/- 0.21 to 4.75 +/- 0.44 and 5.13 +/- 0.28 beats/min/mm Hg (p < 0.05 and p < 0.025, respectively), but had no effect at 100 ng/kg/min. BP increased in these rabbits by 11.5, 10, and 23 mm Hg after these three doses. In group I, AII 50 ng/kg/min increased BP by 8 mm Hg, (p < 0.05) and decreased gain from 6.13 +/- 0.32 to 4.75 +/- 0.44 beats/min/mm Hg (p < 0.01). Therefore, AII 50 ng/kg/min equalized baroreflex sensitivity in the two groups. In group II, both losartan (2.5 mg/kg) and enalapril (1 mg/kg) decreased BP by 8.6 +/- 1.0 1.0 and 10.2 +/- 2.1 mm Hg, (p < 0.01), respectively, and increased the gain by 1-2 beats/min/mm Hg; the drugs did not influence baroreflex sensitivity to any significant extent in group I.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1995

Effects of ketanserin on heart rate and blood pressure variability: implications for the effect on the baroreflex mechanisms.

Ketanserin is an antihypertensive drug with affinity to both serotonin S2- and alpha 1-adrenoceptors. The specific effects of ketanserin on the baroreflex are not fully understood. We, therefore, studied baroreflex regulation based on blood pressure (BP) and heart rate (HR) responses to several maneuvers before and after the administration of 2 x 5 mg of ketanserin i.v. both in supine and in standing posture. Seven young healthy volunteers were investigated. We measured spontaneous variability in HR and BP (Finapres), and performed deep inspiration, Valsalva, and lying-to-standing tests. We also used a modified Valsalva maneuver that consist of Deep Inspiration Breath-holding with closed glottis and EXpiration: DIBEX maneuver. From the BP recordings, peripheral resistance (TPR) and stroke volume (SV) were estimated by the Modelflow method. Thirty minutes after the administration of ketanserin, there was no significant change in mean HR, BP, spectral power of HR and BP variability, baroreflex sensitivity, or Valsalva ratio. Thus ketanserin did not affect the cardiac baroreflex mechanism. However, in standing position, SV increased and TPR decreased under the influence of ketanserin, and BP overshoot after the Valsalva and DIBEX maneuver was significantly decreased as well. There was also no reflex recovery of BP during the DIBEX maneuver in three volunteers, who felt faint. These observations indicate that there is a lack of vasoconstriction. We conclude that ketanserin is not a vasodilator but seems to inhibit vasoconstriction.

Adult↗
PubMed1998

UL-FS 49 (zatebradine) does not affect arterial baroreflex in conscious normal or aortic-constricted rats.

Heart-rate reduction is an important element of patient management during cardiac bypass surgery and in therapeutic measures for combating ischemia and relieving pain in patients with angina. UL-FS 49 is a novel bradycardic agent that purportedly acts solely on the sinoatrial node without potentially deleterious effects on arterial pressure and cardiac inotropism. However, little is known about influences of this agent on neuronal tissue and cardiovascular reflexes. Moreover, left ventricular hypertrophy, which often accompanies cardiovascular disease, is known to attenuate the arterial baroreflex and could have effects interactive with those of UL-FS 49. In this study, the effects of UL-FS 49 on the arterial baroreflex were tested in normal rats (N), rats with left ventricular hypertrophy 14 days after abdominal aortic constriction (AC), and sham-operated controls (SH). Arterial baroreflex sensitivity (BRS) was estimated as the slope of the relation between mean arterial pressure (independent variable) and the RR interval (dependent variable). At the time of study, the AC group had significantly greater mean arterial pressure than either SH or N (159 +/- 2, 122 +/- 3, and 124 +/- 3 mm Hg, respectively; mean +/- SEM, p < 0.01) and significantly greater left ventricular mass to body mass ratio than did SH (3.73 +/- 0.11, 2.33 +/- 0.11 mg/g; p < 0.01). As expected, BRS was significantly depressed in AC, compared with either SH or N (0.52 +/- 0.16, 1.48 +/- 0.12, 1.69 +/- 0.25 ms/mm Hg, respectively; p < 0.01). Despite its potent dose-dependent bradycardic effects in all three groups, UL-FS 49 did not affect BRS significantly in any group. These results show that the arterial baroreflex is largely unaffected by UL-FS 49 in both normal rats and rats with systemic hypertension and left ventricular hypertrophy.

Animals↗
PubMed2003

Parametric system identification of arterial baroreflex with random perturbation of blood pressure in normal subjects.

The purpose of the study was to evaluate the dynamic nature of heart rate baroreflex under closed-loop conditions. We applied pressure perturbation with a random-interval cuff inflation to parametric system identification of the baroreflex. In 10 healthy men (six young, 27 +/- 3.9 years old, and four older, 50 +/- 3.8 years old), blood pressure variations were produced by a random-interval (0.06-0.50 Hz) cuff inflation around bilateral thighs to identify characteristics of the baroreflex with an autoregressive moving average model with exogenous input. The model faithfully described the dynamic relationship between mean blood pressure and RR interval. A theoretical 1 mmHg step input of mean blood pressure caused a rapid increase in RR intervals toward the steady state within 10 s in younger subjects. In older subjects, however, the step response showed a delayed and gradual increase in RR interval over 20 s. The steady-state gain obtained from the autoregressive moving average model with exogenous input was significantly greater than that determined from the slope of the pressure-RR relationship. The conclusion was that the dynamic baroreflex gain was quantified using a parametric system identification technique and blood pressure perturbation by means of a random-interval cuff inflation. This method would potentially be of great use in helping us gain insights into a closed-loop system of complex and dynamic cardiovascular regulation in humans.

Adult↗
PubMed2004

An association between ethanol-evoked enhancement of c-jun gene expression in the nucleus tractus solitarius and the attenuation of baroreflexes.

BACKGROUND: An increased expression of Fos, the protein product of the immediate early gene c-fos, in the nucleus tractus solitarius (NTS) is associated with dysfunction in baroreceptor reflex control of heart rate. Our previous studies demonstrated that ethanol attenuates baroreflex sensitivity (BRS) in rats and humans. In this study, we tested the hypothesis that enhanced expression of the immediate early gene c-jun (an index of neuronal activity) in the NTS contributes to the baroreflex dysfunction caused by ethanol. METHODS: Conscious male spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats were used to measure blood pressure, heart rate, and baroreflex sensitivity (Oxford method). The c-jun messenger RNA (mRNA) expression in NTS was measured by in situ hybridization. RESULTS: Ethanol elicited dose-dependent attenuation in BRS in WKY rats, which was associated with significant increases in c-jun mRNA in the NTS. In contrast, ethanol had no effect on BRS or c-jun mRNA in the NTS of the SHRs; the latter exhibited significantly lower BRS and higher c-jun mRNA in the NTS compared with WKY rats. CONCLUSIONS: An increased basal level of c-jun mRNA in the NTS may contribute to the reduced BRS in the SHR, and ethanol enhancement of neuronal activity of the NTS, expressed as increased c-jun mRNA expression, may contribute to its attenuation of BRS, which highlights the NTS as a neuroanatomical target for ethanol action on baroreflexes.

Animals↗