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PubMed1994

Short-term effects of naloxone on hemodynamics and baroreflex function in conscious dogs with pacing-induced congestive heart failure.

OBJECTIVES: The purpose of this study was to determine the effects of naloxone on systemic hemodynamics and reflex function in dogs with congestive heart failure induced by rapid pacing. BACKGROUND: We have shown previously that naloxone, an opiate receptor antagonist, improves cardiac output, aortic blood pressure, systolic performance and the baroreflex function in conscious dogs with chronic right-sided congestive heart failure. However, whether endogenous opioids also play a role n mediating the reduction of myocardial and baroreflex function in animals with left heart failure remains controversial. METHODS: We administered naloxone (1 mg/kg body weight) and normal saline solution to 15 dogs with pacing-induced congestive heart failure (225 beats/min for 8 weeks) and 11 control dogs. In addition to systemic hemodynamic measurements, the slope of pressure-area relation obtained from echocardiography with intravenous bolus injection of phenylephrine was taken as a load-independent index of myocardial contractility. Baroreflex function was estimated by the slope of the regression line relating systolic aortic pressure and RR interval. RESULTS: Plasma beta-endorphin levels were elevated in dogs with congestive heart failure. Naloxone administration increased heart rate, mean aortic pressure, first derivative of left ventricular pressure, cardiac output and myocardial contractility in pacing-induced congestive heart failure. These changes correlated significantly with basal plasma beta-endorphin levels and were accompanied by increases in plasma beta-endorphin and catecholamines after naloxone administration. However, unlike the hemodynamic and cardiac effects of naloxone, baroreflex function did not change after naloxone in dogs with congestive heart failure. CONCLUSIONS: The increase in basal plasma beta-endorphin suggests that the endogenous opiate system is activated in left-sided congestive heart failure. Because naloxone improves the systemic hemodynamics and myocardial contractile function under this condition, the endogenous opioids appear to play an important role in mediating the myocardial depression that occurs in heart failure. However, the endogenous opiate system has no apparent effect on the regulation of baroreflex control in heart failure induced by rapid pacing.

Animals↗
PubMed2005

Reduced baroreflex effectiveness index in hypertensive patients with chronic renal failure.

BACKGROUND: Impaired arterial baroreflex function has been associated with an increased risk of ventricular arrhythmia and sudden death. This has also been suggested for patients with chronic renal failure (CRF) who are at high risk for cardiovascular morbidity. The aim of this study was to investigate the arterial baroreflex function in CRF patients with emphasis on analyzing the time during which the arterial baroreflex is active, the baroreflex effectiveness index (BEI). METHODS: Beat-to-beat blood pressure (measured with Portapres) and electrocardiography were continuously registered during 30 min rest in 216 hypertensive CRF patients on hemodialysis (n=95), continuous ambulatory peritoneal dialysis (n=59), or conservative treatment (n=59). The spontaneous sequence method was used to calculate BRS and BEI. Age-matched healthy subjects (n=43) were examined for comparison. RESULTS: The BRS was reduced by 51% and the BEI by 49% in CRF patients compared with healthy subjects (P<.001 for both). In addition, CRF patients with diabetes showed further reductions compared with patients without diabetes (15% reduction of BRS and 44% of BEI, P<.01 for both). The treatment modality for renal failure had no effect on BRS or BEI. In a multivariate linear regression analysis, age, body mass index, and systolic blood pressure were independent predictors of BRS, whereas age and diabetes were independent predictors of BEI in patients with CRF. CONCLUSIONS: We conclude that BEI, which is markedly reduced in hypertensive patients with CRF, may convey information on arterial baroreflex function that is complementary to BRS.

Antihypertensive Agents↗
PubMed2004

Effect of vitamin E on carotid artery elasticity and baroreflex gain in young, healthy adults.

In this study we tested the hypothesis that dietary vitamin E supplementation can improve carotid artery elasticity and cardio-vagal baroreflex gain in young, healthy individuals. A total of 20 subjects were studied in a double-blind, placebo-controlled, randomized study. Subjects in the active treatment group received 700 IU/day vitamin E for 1 month. Each subject was studied three times: before, during and 1 month after treatment. Plasma vitamin E levels were determined using high-performance liquid chromatography. Carotid artery diameter was measured by ultrasound and radial artery pressure by tonometry. Baroreflex function was assessed by time and frequency domain spontaneous indices. Plasma vitamin E levels increased by 123%, which was associated with a 20% increase in carotid artery compliance and a 30-60% increase in baroreflex indices. All these changes regressed 1 month after cessation of vitamin E supplementation. Significant correlations were observed across conditions (control, treatment and recovery), among plasma vitamin E concentrations, carotid artery compliance and distensibility values and two of the baroreflex gain indices in the treatment group. Our results demonstrate that vitamin E supplementation can increase carotid artery compliance and baroreflex gain in young, apparently healthy adults.

Adult↗
PubMed2005

Characterization of baroreflex gain in the domestic pigeon (Columba livia).

Birds have a remarkable capacity to regulate circulation yet little is known about the avian baroreflex. Although both linear regression and curve-fitting techniques are frequently used to assess baroreflex function in mammals, only the former technique has been used in birds. We characterized baroreflex gain in domestic pigeons (Columba livia) and compared gain values derived from applying linear regression to ramp changes in mean arterial pressure (MAP) to values derived from fitting a four-parameter sigmoidal function to steady-state alterations in MAP. We found that, unlike mammals, pigeons do not display circadian patterns in MAP, HR or gain derived from bolus injections of vasoactive drugs. The pressor, but not depressor response, was attenuated by administration of the NMDA-antagonist ketamine, suggesting that central processing of the baroreflex may be similar in birds and mammals despite anatomical differences in arterial baroreceptive zones. Because graded infusions of vasoactive drugs could not consistently produce a plateau in the HR response, fitting data to a sigmoidal curve was difficult. Thus, we propose that variations of the Oxford method and linear regression analysis are superior method to assess baroreflex gain in pigeons than curve fitting.

Animals↗
PubMed2006

Aspirin restores normal baroreflex function in hypercholesterolemic rats by its antioxidative action.

Besides its well-known effects on platelet aggregation, aspirin has been suggested to be an antioxidant and is also known to improve the lipid profile. In the present study we tested the hypothesis that aspirin by its antioxidant effect, improves haemodynamic profile and baroreflex sensitivity in rat model of hypercholesterolemia. Hypercholesterolemia was induced in Wistar rats by feeding 1% cholesterol rich diet for 10 weeks. Lipid profile, lipid peroxidation and reduced glutathione were estimated in serum. Haemodynamic changes and baroreflex were measured in anaesthetized rats. Hypercholesterolemic rats showed significant increase in total cholesterol, low-density lipoprotein-cholesterol (LDL-C), very low-density lipoprotein-cholesterol (VLDL-C) and atherogenic index and significant decrease in high-density lipoprotein-cholesterol (HDL-C). Significant rise in blood pressure, heart rate and attenuation of baroreflex sensitivity were also found in hypercholesterolemic rat. Aspirin in the dose of 100 mg/kg showed significant decrease in total cholesterol, LDL-C, VLDL-C and atherogenic index and significant increase in HDL-C. Aspirin treatment prevented the rise in blood pressure, heart rate and significantly improved baroreflex sensitivity in hypercholesterolemic rats. Hypercholesterolemic rats showed free radical generation, evident by a significant increase in serum lipid peroxidation and significant reduction in serum reduced glutathione content. Aspirin treatment significantly decreased lipid peroxidation and significantly increased reduced glutathione content. We have demonstrated that aspirin improves baroreflex response and prevents the rise in blood pressure and heart rate possibly by reducing sympathetic activity due to its antioxidant effect in experimentally induced hypercholesterolemic rats.

Animals↗
PubMed2004

Effect of chronic stress on the cardiac baroreflex in the post-weanling rat.

There is increasing evidence that early life stressors may program blood pressure control mechanisms such that the risk for cardiovascular disease in later life is increased. In the present investigation, the effect of repeated restraint/heat stress during the two-week period immediately after weaning on baroreflex function was determined and the contribution of brain angiotensin II (ANG II) to the changes was assessed in young, conscious, freely moving Sprague Dawley rats. In rats two weeks post weaning, basal MAP was significantly higher and basal HR significantly lower than rats tested immediately after weaning. This change in the operating point of HR was not accompanied by any changes in baroreflex function. Treatment with chronic icv infusion of losartan, an AT1 receptor antagonist, during the two-week period prevented the changes in basal MAP and HR. Chronic stress during the two weeks post weaning, whether due to surgical implantation of icv cannulae or due to restraint/heat stress, significantly shifted the set-point of the baroreflex function to a higher pressure. Chronic icv infusion of losartan during the period prevented these effects (at least in the case of stress due to the presence of icv cannulae) suggesting a role for brain ANG II in the change. Changes in the expression of CRH mRNA in the paraventricular nucleus could not explain the stress-related change in baroreflex function. If the rightward shift in the baroreflex persists into adulthood, it could increase the susceptibility to cardiovascular diseases such as hypertension.

Age Factors↗
PubMed1998

Modulation of baroreflex sensitivity by the state of protein tyrosine phosphorylation in the brainstem of the rat.

Evidence accumulated recently suggests that protein tyrosine phosphorylation may play an important role in regulating neuronal functions. In the present study, we investigated if the state of protein tyrosine phosphorylation in the brainstem regulates baroreflex sensitivity. Anti-phosphotyrosine immunoblots of brainstem tissue revealed that several phosphotyrosine-containing proteins were present in the brainstem and their level of tyrosine phosphorylation was decreased by treatment of the slices with the protein tyrosine kinase (PTK) inhibitor genistein, and increased by treatment with the protein tyrosine phosphatase (PTP) inhibitor pervanadate. In urethane-anaesthetized rats, we found that inhibiting PTK activity by topical application of genistein to the dorsal surface of the medulla reduced the phenylephrine-induced baroreflex bradycardiac response. Conversely, the baroreflex response was potentiated by activating endogenous PTK activity with insulin or by inhibiting PTP activity with pervanadate. Thus these results suggest that the state of cellular tyrosine phosphorylation within the dorsal medulla of the brainstem may regulate the baroreflex control of heart rate, thereby providing the first evidence for a role for protein tyrosine phosphorylation, a key process involved in diverse intracellular signalling pathways, in modulating baroreflex sensitivity.

Animals↗
PubMed1998

Modulatory effects of endothelin on baroreflex activation in the nucleus of the solitary tract.

In this study, we determine the effects of endogenous endothelin on baroreflex activation. After control baroreflex slopes were obtained, the animals received bilateral intra-nucleus tractus solitarii microinjections of saline, or equimolar doses (4 pmol/60 nl) of the endothelin ETA receptor antagonist cyclo (D-Trp-D-Asp-Pro-Val-Leu (BQ-123), Homopiperinidinyl-CO-Leu-D-Trp(CHO)-D-Trp-OH (BQ-610), or the endothelin ETB receptor antagonist N-cis-2,6-dimethylpiperidinocarbonyl-L-gamma-MeLeu-D-Trp( COOCH3)-D-Nle (BQ-788). Intra-nucleus tractus solitarii administration of BQ-123 resulted in a brief initial pressor effect followed by hypotension which resolved by 15 min. The baroreflex slope was significantly enhanced when tested 15 min after BQ-123 treatment (from 2.4 +/- 0.5 ms/mmHg to 3.5 +/- 0.4 ms/mmHg). Similar effects were observed with the other endothelin ETA receptor antagonist, except that the hypertensive and hypotensive responses were more pronounced while the baroreflex slope was similarly increased. In contrast, the endothelin ETB receptor antagonist did not evoke appreciable changes in hemodynamics or in baroreflex slopes. Our results support the concept that endothelin prominently affects reflex cardiovascular function through the endothelin ETA receptor subtype.

Animals↗
PubMed1998

[Prognostic evaluation of post-infarction patients using two-dimensional echocardiography, late ventricular potentials and baroreflex sensitivity].

BACKGROUND: Although many variables are useful predictors of post-infarction mortality, their predictive positive values are weak when applied individually. The aim of this study was to determine the prognostic value of the combination of left ventricular ejection fraction, ventricular late potentials and baroreflex sensitivity. PATIENTS AND METHODS: We studied 69 consecutive post-infarction patients. On the day of their discharge from the coronary unit, all patients underwent a two-dimensional echocardiography, to determine the ejection fraction as well as a high resolution electrocardiogram to detect late potentials. To a subset of 49 patients was carried out to learn their baroreflex sensitivity. The patients were followed for 14 +/- 7 months and the following cardiac end points were considered: sudden cardiac death, non sudden cardiac death and non-fatal episodes of sustained ventricular tachycardia or ventricular fibrillation. RESULTS: There were 8 end points: 3 sudden cardiac deaths, 3 non sudden cardiac deaths and 2 successfully resuscitated sustained ventricular tachycardia episodes. The rate of fibrinolysis was 55%. An ejection fraction < 45%, the presence of late potentials and a baroreflex sensitivity < 3.0 msec/mmHg were univariate predictors with predictive positive values of 33%, 24% and 16%, respectively. When ejection fraction < 45%, late potentials and baroreflex sensitivity < 3.0 were combined, we found a significant increase in the positive predictive value (50%). CONCLUSION: The combined determination of ejection fraction, ventricular late potentials and baroreflex sensitivity allows us to identify subset postinfarction patients with a high rate of cardiac complications.

Aged↗
PubMed1998

Valsalva manoeuvre can be used to study baroreflex sensitivity in pregnancy.

OBJECTIVE: The aim of this study was to assess whether baroreflex sensitivity can be measured in a non-invasive manner with the Valsalva manoeuvre in pregnancy. STUDY DESIGN: Baroreflex sensitivity was measured from the reflex response to phenylephrine injection and phase four of the Valsalva manoeuvre in nine pregnant women at 27 (range 24-33) gestational weeks. RESULTS: Both the phenylephrine test and the Valsalva manoeuvre yielded similar estimates of baroreflex sensitivity (9.3 (4.1) ms/mmHg vs. 8.0 (5.2) ms/mmHg, Pearson's correlation coefficient r = 0.81, P < 0.008, linear regression BRSValsalva (ms/mmHg) = 1.03 x BRSPhenylephrine + 1.59). Comparable changes in heart rate and blood pressure were obtained with the phenylephrine test and the Valsalva manoeuvre. CONCLUSION: The physiological challenge caused by the Valsalva manoeuvre can be used to measure baroreflex sensitivity in pregnancy. A possibility to study baroreflex function non-invasively, without pharmacological intervention, benefits future research of blood pressure regulation in pregnancy.

Adult↗
PubMed2002

Arterial baroreflex and peripheral chemoreflex function after radiotherapy for laryngeal or pharyngeal cancer.

PURPOSE: Denervation of the carotid sinus causes baroreflex and chemoreflex failure, resulting in labile hypertension and loss of hypoxic responsiveness. We investigated whether radiation therapy for laryngeal or pharyngeal cancer affects baroreflex and chemoreflex function. METHODS AND MATERIALS: Twelve patients were studied after radiation therapy for locally advanced laryngeal or pharyngeal cancer (11 male, 1 female, age: 56.0 +/- 7.9 years), 3.3 years (median; range 1.0-4.7) after radiotherapy and 15 healthy controls (11 male, 4 female, 53.4 +/- 9.2 years). We measured baroreflex sensitivity (phenylephrine), blood pressure level and variability (24-h Spacelabs and 5-h Portapres recordings), responses to cardiovascular reflex tests, and the ventilatory responses to normocapnic and hypercapnic hypoxia. RESULTS: Baroreflex sensitivity was lower in patients (9.7 +/- 7.8 ms/mm Hg) than in controls (17.5 +/- 10.3 ms/mm Hg, p = 0.011). Mean office blood pressure was significantly higher in patients (141.5 +/- 27.8/89.2 +/- 10.6 mm Hg, 63.3 +/- 12.3 bpm) than in controls (117.3 +/- 10.1/75.1 +/- 6.8 mm Hg, 61.8 +/- 10.8 bpm). Blood pressure variability was not different between groups, nor were the responses to reflex tests. The normo/hypercapnic ventilatory response to hypoxia was similar in patients (0.21 +/- 0.10/1.37 +/- 0.60 L/min/%) and controls (0.22 +/- 0.16/1.19 +/- 0.78 L/min/%). CONCLUSIONS: Radiation therapy for laryngeal or pharyngeal carcinoma does not affect chemoreflex function, but results in an attenuated baroreflex sensitivity. Clinically relevant blood pressure lability is absent however.

Baroreflex↗
PubMed1997

Impaired baroreflex sensitivity is correlated with hemodynamic deterioration of sustained ventricular tachycardia.

OBJECTIVES: The goal of this study was to evaluate clinical and autonomic variables (heart rate variability and baroreflex sensitivity) related to hemodynamic tolerability of VT in patients with sustained monomorphic VT and a healed myocardial infarction. BACKGROUND: Sustained ventricular tachycardia (VT) with hemodynamic deterioration is associated with a worse prognosis than that of well tolerated VT. The causes of hemodynamic deterioration of VT are incompletely understood. METHODS: Twenty-four consecutive patients with sustained monomorphic VT and a healed myocardial infarction (mean age +/- SD 66 +/- 8 years, left ventricular [LV] ejection fraction 37 +/- 11%) were assigned to group 1 if the VT was well tolerated (n = 11) or to group 2 if faintness or syncope occurred or if systolic blood pressure was < 90 mm Hg with clinical signs of shock (n = 13). RESULTS: No difference was found between the two groups in age, LV function, rate and duration of the VT or heart rate variability. However, patients in group 2 had a significantly lower baroreflex sensitivity (3.4 +/- 1.1 vs. 7.1 +/- 3.7 ms/mm Hg, p = 0.003). Multiple logistic regression analysis showed that only the value of baroreflex sensitivity (p = 0.0003)-but not age, LV ejection fraction, VT cycle length or SD of the RR interval (all p > 0.25)-correlated with the tolerability of the VT. Finally, LV ejection fraction (p = 0.0001) and baroreflex sensitivity (p = 0.0003)-but not age, cycle length of the tachycardia or SD of the RR interval-predicted cardiac death or unstable VT during follow-up. CONCLUSIONS: These data suggest that an impaired cardiovascular reflex response may play a key role in the hemodynamic deterioration of sustained VT and that the evaluation of baroreflex sensitivity in patients at high risk for sustained VT may become useful both in risk stratification and in the individualization of treatment.

Aged↗
PubMed1998

Reduced cardiopulmonary baroreflex sensitivity in patients with hypertrophic cardiomyopathy.

OBJECTIVES: We sought to assess baroreflex function in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: We have previously demonstrated a specific abnormality in the afferent limb of the cardiopulmonary baroreflex in patients with vasovagal syncope. Patients with HCM exhibit abnormal control of their vasculature during exercise and upright tilt; we therefore hypothesize a similar abnormality in the afferent limb of the cardiopulmonary baroreflex arc. METHODS: We investigated 29 patients with HCM and 32 control subjects. Integrated baroreceptor sensitivity was assessed after administration of phenylephrine. Cardiopulmonary baroreceptor sensitivity was assessed by measuring forearm vascular resistance (FVR) during lower body negative pressure (LBNP). Carotid artery baroreflex sensitivity was assessed by measuring the in RR interval during manipulation of carotid artery transmural pressure. The integrity of the efferent limb of the reflex arc was determined by studying responses to both handgrip and peripheral alpha-receptor sensitivity. RESULTS: During LBNP, FVR increased by only 2.36+/-9 U in patients, compared with an increase of 123+/-8.76 U in control subjects (p=0.001). FVR paradoxically fell in eight patients, but in none of the control subjects. Furthermore, FVR fell by 4.9+/-5.6 U in patients with a history of syncope, compared with an increase of 4.7+/-7.2 U in those without syncope (p=0.014). Integrated and carotid artery baroreflex sensitivities were similar in patients and control subjects (14+/-7 vs. 14+/-6 ms/mm Hg, p=NS and -3+/-2 vs. -4+/-2 ms/mm Hg, p=NS, respectively). Similarly, handgrip responses and the dose/response ratio to phenylephrine were not significantly different. CONCLUSIONS: This study suggests that patients with HCM have a defect in the afferent limb of the cardiopulmonary reflex arc.

Adult↗
PubMed1998

Arterial baroreflex impairment in patients during acute coronary occlusion.

OBJECTIVES: We tested whether acute coronary occlusion interferes with arterial baroreceptor control of heart rate in humans. BACKGROUND: Subnormal baroreflex sensitivity (BRS) is an important risk indicator for sudden death. Animal research indicates that both chronic myocardial infarction and acute coronary occlusion impair baroreflex modulation of heart rate. METHODS: We measured RR interval prolongation after phenylephrine-induced systolic pressure increases before and during 2-min coronary occlusions in 47 patients (27 men) undergoing clinically indicated single-vessel coronary angioplasty for stenoses in the proximal or midportion of the vessel causing >50% reduction in the arterial diameter, with normal antegrade flow (33 anterior descending, 10 circumflex, 4 right coronary artery). A control group of 11 patients treated for chronic total occlusion of a coronary artery was assessed to evaluate nonspecific changes in baroreflex function during a 2-min balloon inflation in the occluded artery. RESULTS: The BRS decreased from 5.2+/-3.8 (mean+/-SD) to 4.1+/-3.5 ms x mm Hg(-1) (p=0.01) during the coronary occlusion in the 28 patients with preserved arterial baroreceptor control of heart rate-that is, adequate blood pressure responses and correlation coefficients of the slopes both in baseline and during coronary occlusion. The same phenylephrine dose increased systolic pressure less during than before coronary artery occlusion (21+/-21 versus 36+/-16 mm Hg, p < 0.0001), and in 6 patients it failed to prevent systolic pressure reduction during occlusion. Correlation coefficients of the baroreflex regressions decreased from 0.81+/-0.27 to 0.47+/-0.44 (p < 0.0001) during coronary artery occlusion in the 41 patients with adequate systolic pressure rises in both phenylephrine tests, and the association between RR intervals and rising systolic pressures was lost in 13 patients during coronary occlusion. Balloon inflation in a chronic total occlusion of a coronary artery did not cause significant changes in BRS (from 5.3+/-4.0 to 5.2+/-3.7 ms x mm Hg(-1)), correlation coefficient of the slope or phenylephrine-induced pressure rise. CONCLUSIONS: Our study shows that abrupt coronary occlusion impairs baroreflex modulation of vagal and sympathetic nervous outflow in humans.

Acute Disease↗
PubMed2002

Orthostatic tolerance and spontaneous baroreflex sensitivity in men versus women after 7 days of head-down bed rest.

Many factors are involved in the development of orthostatic intolerance after real or simulated weightlessness. The aim of our study was to compare the effects of 7-day head-down bed rest (HDBR) in eight women and eight men on the spontaneous baroreflex sensitivity (standard spectral method and new time-frequency algorithm) during lower body negative pressure (LBNP) tests. Results obtained before HDBR have shown in women, compared to men, higher heart rate, lower blood pressure, higher parasympathetic modulation at rest and greater decrease in baroreflex sensitivity with greater increase in sympathetic activity during LBNP. After HDBR, we observed in both men and women a dramatic decrease in orthostatic tolerance (7.0 min at R + 1 vs. 10.0 min, p<0.05, at BDC-1 in men; 5.4 vs. 9.0 min, p<0.05, in women) together with a decrease in plasma volume (-9.1 +/- 0.9% in men, -9.5 +/- 1.4% in women) and in spontaneous baroreflex sensitivity without gender effect. After HDBR, at the highest level of LBNP, diastolic blood pressure increased in men (+5.6 +/- 1.3 mm Hg) and decreased in women (-1.0 +/- 2.7 mm Hg) with a gender difference (p<0.05). This result suggests impaired vasoconstriction in women after HDBR. Neither endocrine response nor alterations to the cardiac baroreflex can explain gender differences in orthostatic tolerance after HDBR as reported by previous studies. Further studies need to be conducted in order to obtain a more precise analysis of gender difference in arteriolar vasoconstriction after HDBR. The time frequency method we developed to study changes in spontaneous baroreflex might be applied to the analysis of LBNP tests.

Adult↗
PubMed2003

Effect of water immersion on renal sympathetic nerve activity and arterial baroreflex in conscious rabbits with heart failure.

Several studies have indicated an interaction between cardiopulmonary mechanoreflex and arterial baroreflex. However, the contribution of cardiopulmonary mechanoreflex to an abnormal arterial baroreflex in chronic heart failure (CHF) has not been fully investigated. We examined the effect of the activation of cardiopulmonary mechanoreceptors induced by head-out water immersion (WI) on the arterial baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) in conscious rabbits with CHF induced by myocardial infarction. The arterial baroreflex sensitivity (BRS) of both HR and RSNA were decreased in CHF. WI induced a small decrease in RSNA in CHF compared to a sham-operated group (Sham), despite a similar increase in central venous pressure. WI did not affect BRS of HR or RSNA in either Sham or CHF. By averaging rectified RSNA recordings, we found that miniature RSNA in the control in CHF was higher than that in Sham. WI decreased the synchronized RSNA without changing miniature RSNA in either group. These results suggest that cardiopulmonary mechanoreflex control of RSNA is reduced in CHF, and that cardiopulmonary mechanoreflex has little effect on arterial baroreflex. An increase in miniature RSNA may reflect sympatho-excitation in CHF.

Adrenergic Fibers↗
PubMed2003

Effects of heat stress on baroreflex function in humans.

INTRODUCTION: Heat stress significantly reduces orthostatic tolerance in humans. The mechanism(s) causing this response remain unknown. The purpose of this review article is to present data pertaining to the hypothesis that reduced orthostatic tolerance in heat stressed individuals is a result of heat stress induced alterations in baroflex function. METHODS: In both normothermic and heat stressed conditions baroreflex responsiveness was assessed via pharmacological and non-pharmacological methods. In addition, the effects of heat stress on post-synaptic vasoconstrictor responsiveness were assessed. RESULTS: Generally, whole body heating did not alter baroreflex sensitivity defined as the gain of the linear portion of the baroreflex curve around the operating point. However, whole body heating shifted the baroreflex curve to the prevailing (i.e. elevated) heart rate and muscle sympathetic nerve activity. Finally, the heat stress impaired vasoconstrictor responses to exogenous administration of adrenergic agonists. CONCLUSION: Current data do not support the hypothesis that reduced orthostatic tolerance associated with heat stress in humans is due to impaired baroreflex responsiveness. This phenomenon may be partially due to the effects of heat stress on reducing vasoconstrictor responsiveness.

Baroreflex↗
PubMed2003

Clonidine improves postprandial baroreflex control in familial dysautonomia.

BACKGROUND: Patients with familial dysautonomia (FD) frequently experience hypertensive crises after gastrostomy feeding. The central alpha2-agonist clonidine attenuates feeding-induced crises. The aim of this study was to assess the effect of clonidine on cardiovascular autonomic modulation and particularly baroreflex sensitivity in familial dysautonomia after gastrostomy feeding. MATERIAL AND METHODS: In nine patients, we monitored the RR-interval and systolic blood pressure at supine rest before (baseline 1) and after gastrostomy feeding (GF1). One day later, recordings were repeated after clonidine intake (baseline 2, GF2). We determined spectral powers of RR-interval and systolic blood pressure in the low- (LF) and high-frequency range (HF). Sympathovagal balance was determined from the LF/HF ratio of RR-interval. Baroreflex sensitivity was assessed from the alpha-index of systolic blood pressure and RR-interval. RESULTS: Gastrostomy feeding decreased RR-interval, while systolic blood pressure remained stable. Clonidine induced higher RR-intervals before and after gastrostomy feeding but decreased systolic blood pressure at baseline only. Gastrostomy feeding decreased HF-power of RR-interval significantly without clonidine, but only slightly after premedication. Clonidine increased the HF-power of RR-interval slightly at baseline and significantly after gastrostomy feeding. Gastrostomy feeding increased the LF/HF ratio without clonidine only. Clonidine decreased the LF/HF ratio at baseline and after gastrostomy feeding. Gastrostomy feeding did not change baroreflex sensitivity, but baroreflex sensitivity was higher at visit 2 than visit 1. CONCLUSIONS: In familial dysautonomia, clonidine augments baroreflex sensitivity and parasympathetic modulation. The resulting cardiovascular stabilization might attenuate feeding-induced crises.

Adolescent↗