Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Baroreflex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 415 records · Page 23Linked to original sources
PubMed2001

Spontaneous baroreflex sensitivity as a dynamic measure of cardiac anticholinergic drug effect.

1. In this study, the analysis of spontaneous baroreflex sensitivity (BRS) was applied to the dynamic assessment of cardiac anticholinergic drug effect in healthy male volunteers. 2. The anticholinergic effects of single intravenous (i.v.) injections of atropine (10 microg kg(-1)), glycopyrrolate (5 microg kg(-1)) and scopolamine (5 microg kg(-1)), as well as a 2-h infusion of glycopyrrolate (5 microg kg(-1) h(-1)) were investigated. Baroreflex sensitivity, a validated measure of cardiac parasympathetic reflex regulation, was repeatedly measured from 5-min recordings of electrocardiogram (ECG) and continuous blood pressure by using the sequence technique, a method based on detection of spontaneous fluctuations in blood pressure and heart rate. 3. Single injections of atropine, glycopyrrolate and scopolamine decreased the mean BRS by 71 +/- 32, 68 +/- 23 and 27 +/- 45%, respectively, whereas the slow glycopyrrolate infusion gradually decreased BRS (up to 83 +/- 11% reduction) and increased both systolic (SAP) and diastolic arterial pressures (DAP) (on an average, by 9 mmHg). 4. During the withdrawal of the parasympathetic blockade (indicated by increasing BRS), the proportion of baroreflex sequences in the recordings increased transiently from 10 up to 20-25%, probably reflecting the restoration of the baroreflex integrity and the baroreflex-induced attempt to counteract the blood pressure increase. 5. The sequence method to study BRS seems to be feasible in the assessment of cardiac anticholinergic drug effects, and it also provides good time resolution for the dynamic measurements.

Adult↗
PubMed2002

Cardiac baroreflex control in humans during and immediately after brief exposure to simulated high altitude.

To examine the baroreflex response in humans during and immediately after acute hypoxia exposure, the cardiac baroreflex sensitivity (BRS) was studied using adaptation of RR intervals in response to spontaneous systolic blood pressure fluctuations (sequences methodology) in 11 unacclimatized subjects. All measurements were made under fixed breathing rate, and realized consecutively at baseline level (20 min), at an inspired oxygen concentration of 11% (15 min) and again under normoxic conditions (20 min; recovery period). The spontaneous baroreflex response decreases progressively during hypoxic exposure, causing a tachycardic response at this FiO2 without any significant alteration of the systolic or diastolic blood pressure. The magnitude of decrease for this variable at the end of exposure averaged 42.9 +/- 15.6%. The simultaneous spectral analysis of heart rate (HR) variability in hypoxic condition confirmed an alteration in the parasympathetic activity (HFnu: -17.8 +/- 30.9% versus basal conditions, P < 0.01) counterbalanced by an exaggerated sympathetic activity (LFnu: +33 +/- 42.4%, P < 0.05) at the sinus node. Interestingly, we could observe an enhanced cardiac baroreflex response during the period following the inhalation of the hypoxic mixture (+130.6 +/- 15.6% of basal conditions, P < 0.001). There is a relationship with a significant and abrupt increase in the parasympathetic control of HR (mean HR reached 111 +/- 8.1% of the mean basal HR, P < 0.01). These results suggest that brief exposure to hypoxia under rate-controlled ventilation is associated with a significant alteration in the spontaneous cardiac baroreflex. This important cardiac autonomic imbalance is followed by a significant increase in the cardiac parasympathetic drive even after the disappearance of the hypoxic stimulus.

Adaptation, Physiological↗
PubMed1993

The diagnosis and treatment of baroreflex failure.

BACKGROUND: Baroreflexes originate in the great vessels of the neck and thorax and prevent arterial pressure from rising or falling excessively. METHODS: This study was undertaken to clarify the cause, clinical spectrum, and therapy of this disorder. We studied 11 patients with baroreflex failure presenting as severe, labile hypertension and hypotension, often with headache, diaphoresis, and emotional instability, and characterized by the failure of exogenous vasoactive substances to alter heart rate. Each underwent hemodynamic monitoring and biochemical, physiologic, and pharmacologic testing. RESULTS: The patients' maximal systolic blood pressures ranged from 164 to 280 mm Hg, and their minimal systolic pressures ranged from 58 to 96 mm Hg. Plasma norepinephrine and epinephrine concentrations were sometimes many times normal during blood-pressure surges. All the patients had excessive pressor and tachycardia responses to the mental-arithmetic and cold pressor tests and marked hypersensitivity to clonidine. The underlying causes of baroreflex failure included the familial paraganglioma syndrome, neck surgery or radiation therapy for pharyngeal carcinoma, bilateral lesions of the nucleus tractus solitarii, and surgical section of the glossopharyngeal nerves; in two patients the cause was unknown. Therapy with clonidine reduced the frequency of attacks by 81 percent and attenuated the elevated blood pressure and heart rate in the attacks that occurred. CONCLUSIONS: The syndrome of baroreflex failure should be considered in patients with otherwise unexplained labile hypertension. Clonidine attenuates the pressor and tachycardic surges in baroreflex failure.

Adult↗
PubMed2002

Baroreflex stimulation shows impaired cardiovagal and preserved vasomotor function in early-stage amyotrophic lateral sclerosis.

OBJECT: In ALS patients, autonomic nervous system dysfunction might account for an additional reduction of the quality and expectancy of life of individual patients and contribute to unexpected early fatalities. This study was undertaken to assess baroreflex-mediated vagal and sympathetic cardiovascular control of the heart and blood vessels in ALS patients. METHODS: In 12 early-stage ALS patients (age 54 +/- 4 years) and 12 controls (age 55 +/- 3 years) we assessed resting baroreflex sensitivity (BRS) by spectral analysis, then stimulated the carotid baroreflex by oscillating neck suction at 0.1 Hz to assess the autonomic modulation of the heart and blood vessels and at 0.2 Hz to assess the effect of parasympathetic stimulation on the heart. RESULTS: Resting heart rate was significantly higher in the ALS patients than in the controls (P < 0.05), but resting baroreflex sensitivity did not differ significantly between the groups. Stimulation at 0.2 Hz induced an oscillation in R-R interval that was significantly smaller (P < 0.05) in ALS patients than in controls. R-R interval responses to 0.1 Hz stimulation were significantly (P < 0.01) reduced in ALS patients compared to controls. Responses of blood vessels to 0.1 Hz stimulation did not differ significantly between the groups. CONCLUSION: In early-stage ALS patients, BRS might be normal at rest. Only baroreflex activation reveals impaired cardiovagal responses while sympathetic vasomotor control is preserved. Treatment to restore sympathetic-parasympathetic balance to the heart could prevent early cardiovascular fatalities in some ALS patients.

Amyotrophic Lateral Sclerosis↗
PubMedDate not supplied

Baroreflex sensitivity in secondary hypertension.

A deranged baroreceptor control of the cardiovascular functions has been reported in essential hypertension. Studies performed in experimental animals and in humans using different approaches have documented an impairment of both baroreflex heart rate modulation (resetting and loss of sensitivity) and baroreceptor control of peripheral vasomotor tone (only resetting). Baroreflex alterations have been reported also in secondary forms of hypertension, but data are controversial. This paper reviews recent works concerning baroreflex function in secondary hypertension. Either structural changes of arterial wall (decrease of vascular distensibility) or functional processes (involving angiotensin II, aldosterone, catecholamines, nitric oxide) have been proposed as potential mechanisms responsible for baroreflex readjustments in secondary hypertension. It remains unclear, and it is difficult to define exactly, if baroreflex changes associated with secondary form of hypertension are primarily due to factors specific for different hypertensive conditions, or merely follow blood pressure elevation.

Adrenal Gland Neoplasms↗
PubMed2003

The influence of one-year treatment by angiotensin converting enzyme inhibitor on baroreflex sensitivity and flow-mediated vasodilation of the brachial artery in essential hypertension--comparison with calcium channel blockers.

BACKGROUND: Both baroreflex sensitivity and flow-mediated vasodilator function have been recognized to have prognostic significance in cardiovascular diseases. Long-term antihypertensive treatment effects on these parameters, however, remain unclear. SUBJECTS AND METHODS: We examined the effects of long-term treatment by angiotensin converting enzyme inhibitors (ACEI) orcalcium channel blockers (CCB) on baroreflex and flow-mediated vasodilator function in patients with essential hypertension (EH). We recruited 36 patients aged 56 +/- 11 years, with systolic blood pressure > or = 160 mmHg and/or diastolic blood pressure > or = 95 mmHg. Patients were assigned either to treatment by long-acting ACEI (n = 12) or CCB (n = 24). All patients were followed for 12 months. Optimal BP was achieved by two optional increases in treatment: dose-doubling of the primary drug during the first three months and the addition of diuretics or beta-blockers thereafter. Target blood pressure was 140/90 mmHg or a fall > or = 20/10 mmHg. Baroreflex sensitivity was examined by spectral analysis of blood pressure and RR interval variabilities before treatment and after 3 and 12 months of treatment. The flow-mediated vasodilator function was determined before and 12 months after treatment by measuring the change in brachial artery diameter during increases in flow induced by reactive hyperemia. RESULTS: Baseline blood pressures were similar between the ACEI and CCB groups (172 +/- 5/103 +/- 2 vs. 172 +/- 4/101 +/- 3 mmHg). Blood pressures after 3 and 12 months of treatment also did not differ between the ACEI and CCB groups (149 +/- 4/91 +/- 2 vs. 145 +/- 2/85 +/- 2 mmHg, and 133 +/- 5/84 +/- 2 vs. 133 +/- 2/81 +/- 2 mmHg, respectively). Baseline baroreflex sensitivity was similar between the groups (6.7 +/- 0.8 vs. 5.9 +/- 0.6 msec/mmHg). This parameter remained unchanged at three months but increased after 12 months of treatment in both the ACEI (9.5 +/- 1.6 msec/mmHg, p = 0.05) and CCB (9.1 +/- 1.2 msec/mmHg, p = 0.006) groups. Percent increases in brachial arterial diameter and flow during reactive hyperemia increased in the group treated with ACEI (12.4 +/- 3.5 vs. 25.8 +/- 6.3% and 618 +/- 72 vs. 953 +/- 166, p < 0.05 for both) but both parameters remained unchanged in the group treated with CCB. CONCLUSION: These data suggest that long-term blood pressure control with modem antihypertensive drugs improves baroreflex function. Treatment with ACEI may be more favorable for flow-mediated vasodilator function than treatment with CCB.

Aged↗
PubMed2004

Gender differences in baroreflex response and heart rate variability in anaesthetized humans.

BACKGROUND: In conscious humans, men have a greater cardiovagal baroreflex gain than women. We studied gender-related differences in baroreflex function during general anaesthesia. METHODS: Sixty healthy patients (30 male and 30 female) were anaesthetized with sevoflurane 2% end-tidal in air and oxygen, and their lungs were mechanically ventilated. We recorded the ECG and invasive arterial pressure. Baroreflex gain was measured as the linear relationship of R-R interval with systolic arterial pressure changes caused by doses of phenylephrine i.v., and also the spontaneous changes in R-R interval and arterial pressure. In addition, consecutive R-R intervals were analysed using a fast Fourier transformation. RESULTS: Baroreflex gains (mean (sd)) assessed by the pharmacological method in men (7.98 (5.12) ms x mm x Hg(-1)) was significantly greater than that in women (4.89 (3.87) ms x mm x Hg(-1)). Similarly, spontaneous baroreflex gains were significantly greater in men than in women, and correlated well with high-frequency power, but not with low-frequency power or low/high ratio, of heart rate variability in both genders. CONCLUSIONS: Our results extend findings in conscious humans to sevoflurane anaesthesia. Men have greater cardiovagal reflex gains than women, which may reflect differences in parasympathetic action on heart rate.

Adult↗
PubMed2006

Validation of a new noninvasive method to measure blood pressure and assess baroreflex sensitivity in preterm infants during sleep.

STUDY OBJECTIVES: Accuracy and precision of a noninvasive device for continuously measuring blood pressure (BP) (Finometer, FMS, The Netherlands) during sleep was assessed in preterm infants. DESIGN: Absolute BP beat-to-beat values, interbeat changes, measurement precision, and baroreflex sensitivity were compared with BP measurements from intraarterial catheters. PARTICIPANTS: Ten preterm infants (gestational age 27-36 weeks; birth weight 964-2620 gm) were studied in the neonatal intensive care unit. MEASUREMENTS AND RESULTS: The 2 modes of BP measurement were compared in 2-minute epochs (n = 10-12/infant). Mean arterial pressure, systolic arterial pressure, and diastolic arterial pressure were analyzed beat to beat, and baroreflex sensitivity was assessed using spontaneous sequence analysis. Mean differences for absolute BP (mm Hg) were as follows: mean arterial pressure, 3 (limits of agreement, -1 to 8); systolic arterial pressure, -4 (-8 to 1); and diastolic arterial pressure, 7 (4 to 10). Mean differences and limits of agreement for interbeat changes were essentially 0 for mean arterial pressure, systolic arterial pressure, and diastolic arterial pressure. Precision (+/- 95% confidence intervals, mm Hg) for the Finometer were mean arterial pressure +/- 7, systolic arterial pressure +/- 8, and diastolic arterial pressure +/- 6. Precision was greater for the arterial catheter (mean arterial pressure +/- 3, systolic arterial pressure +/- 4, and diastolic arterial pressure +/- 4). Baroreflex sensitivity calculated from the Finometer BP was (mean +/- SEM, ms/mm Hg) 1.74 +/- 0.23 and, from the catheter system, BP was 1.56 +/- 0.21 (p value NS). CONCLUSIONS: The Finometer provides accurate measurements of beat-to-beat BP and baroreflex sensitivity. The ability to continuously measure BP and baroreflex sensitivity during sleep in infants may provide vital clues into pathologic conditions associated with impaired autonomic control during sleep.

Baroreflex↗
PubMed1999

Cardiac baroreflex during the postoperative period in patients with hypertension: effect of clonidine.

BACKGROUND: Patients with essential hypertension show altered baroreflex control of heart rate, and during the perioperative period they demonstrate increased circulatory instability. Clonidine has been shown to reduce perioperative circulatory instability. This study documents changes in measures of heart rate control after surgery in patients with essential hypertension and determines the effects of clonidine on postoperative heart rate control in these patients. METHODS: Using a randomized double-blind placebo-controlled design, 20 patients with essential hypertension (systolic pressure >160 mm Hg or diastolic pressure >95 mm Hg for > or =1 yr) were assigned to receive clonidine (or placebo), 6 microg/kg orally 120 min before anesthesia and 3 microg/kg intravenously over 60 min before the end of surgery. The spontaneous baroreflex ("sequence") technique and analysis of heart rate variability were used to quantify control of heart rate at baseline, before induction of anesthesia, and 1 and 3 h postoperatively. RESULTS: Baroreflex slope and heart rate variability were reduced postoperatively in patients given placebo but not those given clonidine. Clonidine resulted in greater postoperative baroreflex slope and power at all frequency ranges compared with placebo (4.9+/-2.9 vs. 2.2+/-2.1 ms/mm Hg for baroreflex slope, 354+/-685 vs. 30+/-37 ms2/Hz for high frequency variability). Clonidine also resulted in lower concentrations of catecholamine, decreased mean heart rate and blood pressure, and decreased perioperative tachycardia and hypertension. CONCLUSIONS: Patients with hypertension exhibit reduced heart rate control during the recovery period after elective surgery. Clonidine prevents this reduction in heart rate control. This may represent a basis for the improved circulatory stability seen with perioperative administration of clonidine.

Analgesics↗
PubMed1993

Improved baroreflex sensitivity in elderly hypertensives on lisinopril is not explained by blood pressure reduction alone.

OBJECTIVE: The major goals of this study were to determine whether lisinopril and nifedipine lowered blood pressure and improved carotid baroreflexes in older hypertensives. DESIGN: The effects of lisinopril at 10-40 mg/day versus nifedipine gastrointestinal therapeutic system (GITS) at 30-90 mg/day on blood pressure and baroreflex sensitivity were studied after 3 weeks each on (1) single-blind placebo, (2) double-blind assignment to either lisinopril or nifedipine, (3) single-blind placebo, and (4) crossover to double-blind lisinopril or nifedipine. Measurements at the end of the four phases included 24-h blood pressure using the Accutracker, laboratory hemodynamics with the Dinamap and impedance cardiography, baroreflex sensitivity with the pneumatic neck chamber, and plasma samples for neurohumoral and metabolic activity. PATIENTS: Thirteen patients aged 55 years or older (mean +/- SEM 65 +/- 1 years) with mild-to-moderate hypertension completed the study. MAIN OUTCOME MEASURES: The primary data for analysis across the four study phases included ambulatory blood pressure values, laboratory hemodynamics, and baroreflex sensitivity. RESULTS: Compared with the preceding placebo, lisinopril and nifedipine lowered 24-h blood pressure significantly. In the laboratory, the effects of both compounds on blood pressure, cardiac output, calculated total systemic resistance, and the stroke volume-pulse pressure relationship, an index of arterial compliance, were similar. Lisinopril was associated with a relative increase in the standing systolic blood pressure compared with nifedipine (P < 0.05). This coincided with an enhanced heart-rate (R-R interval) response to neck pressure, which also decreased carotid transmural pressure, with lisinopril versus nifedipine (P < 0.05). CONCLUSIONS: Lisinopril and nifedipine were both effective as monotherapy for controlling blood pressure in these elderly patients. Despite similar effects on blood pressure and systemic hemodynamics, baroreflex sensitivity in response to a reduction in carotid transmural pressure was greater with lisinopril than with nifedipine.

Aged↗
PubMed1997

Effects of central metformin administration on responses to air-jet stress and on arterial baroreflex function in spontaneously hypertensive rats.

OBJECTIVE: To examine effects of intracerebroventricular (ICV) administration of metformin on the responses to environmental stress and on arterial baroreflex function in conscious spontaneously hypertensive rats (SHR). METHODS: SHR were instrumented with an ICV cannula and prepared for measurements of the mean arterial pressure (MAP), heart rate, and renal sympathetic nerve activity (RSNA) during air-jet stress (AJS). After recovery from a pretreatment AJS period, rats were allocated randomly to ICV administration of either vehicle (saline; n = 9) or 1 mg metformin (which is inactive dose after intravenous administration; n = 8). After stabilization for 1 h, the AJS was repeated. The arterial baroreflex control of the heart rate and RSNA was examined at the end of the experiment. RESULTS: ICV metformin decreased the baseline heart rate (by 88+/-14 beats/min) and RSNA (by 19+/-8%) in the absence of changes in MAP. ICV vehicle did not affect responses to the AJS [change in MAP (deltaMAP) = +11+/-2 mmHg, change in heart rate (deltaHR) = +54+/-9 beats/min, change in RSNA (deltaRSNA) = +37+/-8%), but pressor, tachycardic, and renal sympathoexcitatory responses to the AJS were inhibited significantly by ICV metformin (deltaMAP = +4+/-3 mmHg, deltaHR = -5+/-5 beats/min; deltaRSNA = +11+/-3%). ICV metformin did not affect the arterial baroreflex range, but it did increase the maximal gain of the arterial baroreflex control of heart rate (-1.46+/-0.25 versus 0.67+/-0.13%/mmHg, P= 0.01) and RSNA (-5.04+/-1.10 versus -2.47+/-0.28%/mmHg, P = 0.053). CONCLUSIONS: Central metformin administration attenuated the renal sympathoexcitatory response to environmental stress and increased the gain of the arterial baroreflex control of heart rate and RSNA. These actions may contribute to the antihypertensive effect of metformin.

Animals↗
PubMed2000

Assessment of arterial and cardiopulmonary baroreflex gains from simultaneous recordings of spontaneous cardiovascular and respiratory variability.

OBJECTIVES: In usual models of cardiovascular regulation, arterial pressure drives RR interval through a simple baroreflex, and the influence of respiration is dismissed. We examined the applicability of a trivariate autoregressive model to obtain separate values of the gain of the arterial and non-arterial, i.e. cardiopulmonary, components of the lumped baroreflex, employing spontaneous RR interval, systolic arterial pressure and respiration variability. DESIGN: We studied 30 normal subjects (age 37 +/- 1 years), both at rest and during standing, a condition known to enhance sympathetic activity while reducing venous return. Electrocardiogram was obtained by telemetry, arterial pressure by Finapres and respiration with a piezoelectric respiratory belt Data were acquired with a PC and processed with an ad hoc Windows program. METHODS: We employed an additive and a linear multivariate approach to approximate overall gain of the arterial pressure-heart beat period baroreflex (alphalumped) and of its arterial (alphaart) and non-arterial, i.e. cardiopulmonary (alphacp), components, from continuous beat-by-beat series of RR interval, systolic arterial pressure variability and respiration, without using any non-physiological intervention. RESULTS: The overall baroreflex gain at rest (alphalumped = 23.7 +/- 3.4 ms/mmHg) was subdivided into arterial (alphaart = 5.2 +/- 1.0 ms/mmHg) and cardiopulmonary (alphacp = 18.5 +/- 3.2ms/mmHg) components. During active orthostatism, alphaluumped was diminished to 10.0 +/- 2.2 ms/ mmHg. In addition, standing selectively reduced alphacp to 4.8 +/- 1.3 ms/mmHg, while alphaart was not significantly changed. CONCLUSIONS: A trivariate autoregressive model, that considers explicitly the influence of respiration, can subdivide overall, lumped, arterial pressure-heart period baroreflex gain, into two separate components, alphaart and alphacp. Only the latter is reduced by active orthostatism.

Adult↗
PubMed2000

Comparison of renal sympathetic baroreflex effects of rilmenidine and alpha-methylnoradrenaline in the ventrolateral medulla of the rabbit.

OBJECTIVE: To determine the influence of imidazoline receptors and alpha2-adrenoceptors in the rostral ventrolateral medulla (RVLM) on the renal sympathetic baroreflex. METHODS: The effects of rilmenidine (4 nmol) and alpha-methylnoradrenaline (alpha-MNA, 80 nmol) micro-injected into the RVLM of urethane-anaesthetized rabbits previously implanted with renal nerve recording electrodes were examined before and after micro-injection of the imidazoline receptor/alpha2-adrenoceptor antagonist idazoxan and the alpha2-adrenoceptor antagonist 2-methoxyidazoxan (2-MI). RESULTS: Rilmenidine and alpha-MNA both lowered mean arterial pressure (MAP) by 28% and renal sympathetic nerve activity (RSNA) by 35%, and reduced RSNA upper plateaus and ranges by 30-70%. Rilmenidine decreased both sympathetic burst frequency and amplitude while alpha-MNA reduced amplitude only. Rilmenidine shifted the RSNA baroreflex curve to the left while alpha-MNA shifted the curve to the right Idazoxan (13 nmol) reversed the hypotension and all RSNA effects of rilmenidine, while 2-MI (4 nmol) increased MAP 18% above the control and also reversed all RSNA parameters. By contrast, 2-MI reversed the alpha-MNA-induced hypotension and partially restored RSNA and the upper plateau of the RSNA baroreflex curve. Idazoxan treatment only partially reversed the hypotension after alpha-MNA and had no effect on any of the baroreflex curves. CONCLUSION: Both alpha-MNA and rilmenidine injected into the RVLM of rabbits produce renal sympathetic inhibition, but differences in the location of the baroreflex curve and the pattern of effects on burst amplitude and frequency suggest different mechanisms of action. The effects of idazoxan suggest that rilmenidine acts via imidazoline receptors. Since 2-MI reversed the actions of alpha-MNA and also rilmenidine, this suggests that alpha2-adrenoceptor hypotension can be produced in the rabbit RVLM and that rilmenidine may activate alpha2-adrenoceptors, possibly as a result of activating imidazoline receptors.

Adrenergic alpha-Antagonists↗
PubMed2000

Modulation of the baroreflex control of heart rate by angiotensin-(1-7) at the nucleus tractus solitarii of normotensive and spontaneously hypertensive rats.

OBJECTIVES: In the present study, we evaluated the effect of angiotensin-(1-7) [Ang-(1-7)] and its selective antagonist, D-Ala7-Ang-(1-7) (A-779), at the nucleus tractus solitarii (nTS), in the modulation of the bradycardic component of the baroreceptor reflex. METHODS: Mean arterial pressure (MAP) and heart rate were continuously recorded. Reflex changes in heart rate elicited by bolus injection of graded doses of phenylephrine were evaluated before and after bilateral microinjection (glass micropipette) of Ang-(1-7) (10 pmol or 25 pmol), A-779 (50 pmol) or saline (vehicle) into the nTS of urethane anesthetized male Wistar rats or spontaneously hypertensive rats (SHR). The averaged ratio between reflex changes in heart rate and changes in MAP was used as index of baroreflex sensitivity. RESULTS: Microinjection of Ang-(1-7) into the nTS elicited significant decreases in MAP and heart rate in both Wistar and SHR. While the decrease in MAP was similar in both strains, the changes in heart rate were smaller in SHR. A-779 produced small changes in MAP and heart rate that were no different from those induced by saline. After microinjection of 10 pmol of Ang-(1-7) into the nTS of normotensive rats, there was a significant increase in baroreflex sensitivity. In SHR, only the microinjection of a higher dose (25 pmol) of Ang-(1-7) produced a significant increase in baroreflex sensitivity. A significant reduction inbaroreflex sensitivity was observed after microinjection of A-779 (50 pmol) in both strains. CONCLUSIONS: These results indicate that Ang-(1-7) exerts a tonic modulatory effect on the baroreflex control of heart rate at the nTS, probably through a non-AT1 non-AT2 receptor subtype. In addition, our data showed a reduced sensitivity to Ang-(1-7) at the nTS of SHR, that could be accounting, at least in part, for the decreased baroreflex sensitivity present in this model of hypertension.

Angiotensin I↗
PubMed2001

Spontaneous baroreflex modulation of heart rate and heart rate variability during orthostatic stress in tetraplegics and healthy subjects.

OBJECTIVE: This study was addressed to investigate the contribution of vagal and sympathetic mechanisms to the genesis of low-frequency (LF) oscillations of RR-interval. DESIGN: To this aim, we utilized the pathophysiological model of tetraplegics, who have intact vagal afferent and efferent pathways of the baroreceptor reflex arc but interrupted medullary-spinal sympathetic pathways. METHODS: We studied nine complete, traumatic, tetraplegics (C4-C7, TET) and 10 normally healthy subjects (NR) at rest and during physiological baroreceptors unloading induced by 70 degrees head-up tilt. Autoregressive power spectral analysis was used to investigate RR-interval and systolic arterial pressure (SAP) variabilities. Baroreflex modulation of sinus node was assessed by the spontaneous baroreflex sequences method. RESULTS: Both at-rest and during-tilt LF and high frequency (HF) components were detected in RR-interval of NR, whereas in TET only the HF component was observed in both conditions (with one exception). Baroreflex sensitivity (BRS) did not significantly differ between TET and NR at rest, and underwent a significant and similar decrease during tilt in both groups, being accompanied in NR by a significant increase in LF relative power. Spectral analysis of SAP provided results similar to RR-interval. Tilt also slowed the centre frequency of the LF components of RR-interval and SAP. CONCLUSIONS: During unperturbed physiological conditions, a change in efferent vagal activity to the heart from baroreflex stimulation by spontaneous arterial pressure changes, is unlikely to contribute on its own to the genesis of LF heart period oscillations in humans who lack the ability to modulate sympathetic nerve traffic to the heart. However, the possibility that a baroreflex modulation of LF oscillations require an intact sympathetic control should be carefully considered.

Adult↗
PubMed2003

Baroreflex and chemoreflex function after bilateral carotid body tumor resection.

OBJECTIVE: To investigate whether bilateral carotid body tumor resection invariably and chronically affects arterial baroreflex or peripheral chemoreflex function. METHODS: We studied eight consecutive patients (two men and six women; ages 48.1 +/- 11.8 years), a median time of 3.4 years (range 1.3-20.6 years) after bilateral carotid body tumor resection, and 12 healthy control individuals (eight men and four women; ages 53.7 +/- 10.1 years). Baroreflex sensitivity (phenylephrine), blood pressure and its variability (24 h Spacelabs and 5 h Portapres recordings), responses to standard cardiovascular reflex tests and the ventilatory responses to normocapnic and hypercapnic hypoxia were assessed. RESULTS: Baroreflex sensitivity was lower in patients (6.4 +/- 7.2 ms/mmHg) than in controls (14.7 +/- 6.6 ms/mmHg; P +/- 0.011). Mean office blood pressure and heart rate were normal in patients (123.3 +/- 11.9/79.0 +/- 7.3 mmHg and 67.5 +/- 9.4 beats/min, respectively) and controls (117.8 +/- 10.6/74.0 +/- 6.8 mmHg and 61.1 +/- 9.2 beats/min, respectively). Blood pressure variability was increased during ambulatory measurements. Three patients exhibited orthostatic hypotension. The Valsalva ratio, an index of baroreflex-mediated cardiovagal innervation, was lower in patients (1.4 +/- 0.2) than in controls (1.8 +/- 0.5; P +/- 0.008). The normocapnic ventilatory response to hypoxia was absent in all patients, whereas a small residual response to hypoxia was observed under hypercapnic conditions in two patients. CONCLUSIONS: Bilateral carotid body tumor resection results in heterogeneous expression of arterial baroreflex dysfunction, whereas the normocapnic hypoxic drive is invariably abolished as a result of peripheral chemoreflex failure.

Adult↗
PubMed2003

Sleep-related changes in baroreflex sensitivity and cardiovascular autonomic modulation.

OBJECTIVE: We examined the effects of the various sleep stages on baroreflex sensitivity (BRS), and heart rate and blood pressure (BP) variability, and tested the hypothesis that there is a different behavior of the baroreflex control of the sinus node in response to hypertensive and hypotensive stimuli and in relation to different cycles of the overnight sleep. DESIGN: Polygraphic sleep recordings were performed in 10 healthy males. The BP and the RR interval were continuously recorded during sleep. METHODS: BRS was calculated by the sequences method. Autoregressive power spectral analysis was used to investigate the RR-interval and BP variabilities. RESULTS: During rapid eye movement (REM) sleep BRS significantly increased in response to hypertensive stimuli in comparison with non-rapid eye movement (NREM) sleep and the awake state, whereas it did not change in response to hypotensive stimuli. In the first sleep cycle, BRS significantly increased during NREM in comparison with wakefulness, whereas during REM BRS in response to hypertensive stimuli did not show significant changes as compared with the awake state and/or with NREM. During REM occurring in the sleep cycle before morning awakening, BRS showed a significant increase in response to hypertensive stimuli in comparison with both NREM and the awake state. CONCLUSIONS: During sleep, arterial baroreflex modulation of the sinus node is different in response to hypotensive and hypertensive stimuli particularly during REM. Furthermore, baroreflex control of the sinus node shows a non-uniform behavior during REM occurring in different nocturnal sleep cycles. These findings suggest that the arterial baroreflex is more effective in buffering the increased sympathetic activation associated with REM at the end of sleep than in the early night.

Adult↗
PubMed2004

Altered profile of baroreflex and autonomic responses to lower body negative pressure in chronic orthostatic intolerance.

BACKGROUND: Chronic orthostatic intolerance (COI) is a common and disabling autonomic syndrome of unclear pathophysiology. We tested the hypothesis that baroreflex and autonomic responses to graded lower body suction (LBNP, up to -40 mmHg) could be altered in COI patients. METHODS: Electrocardiogram (ECG), non-invasive arterial blood pressure and respiratory activity were measured during progressive LBNP (seven patients and seven volunteers). Lumped arterial baroreflex sensitivity (alpha index), and its arterial and cardiopulmonary components, were assessed by multivariate closed-loop analysis of RR interval and systolic arterial pressure (SAP) spontaneous variabilities and respiration. Monovariate spectral analysis of RR interval and SAP variability provided markers of autonomic regulation of the sinoatrial (SA) node and of vascular sympathetic modulation. RESULTS: Similar reductions in overall and cardiopulmonary baroreflex gain were observed in both groups in response to graded LBNP. In contrast, only controls demonstrated a selective increase in arterial baroreflex sensitivity, at low-grade LBNP. Clear increases in the low-frequency component of RR interval variability (LFRR) [and decreases in the high-frequency component of RR interval variability (HFRR), both in normalized units] were observed in controls with graded LBNP, while insignificant changes occurred in COI patients, who showed, conversely, exaggerated sympathetic vasomotor responses [as assessed by the low frequency component of SAP variability (LFSAP)]. CONCLUSIONS: Patients with chronic orthostatic intolerance show distinct signs of altered baroreflex and autonomic regulation of the SA node and of the vasculature in response to graded LBNP.

Adult↗