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 775 records · Page 43Linked to original sources
PubMed1992

Long-term calorie restriction enhances baroreflex responsiveness in Fischer 344 rats.

Diet influences many aspects of cardiovascular function. Restriction of caloric intake represents a major nonpharmacological means of reducing blood pressure. The aim of the present work was to determine the effects of long-term calorie restriction on mean arterial pressure (MAP) and baroreflex responsiveness of the conscious, normotensive, nonobese Fischer 344 male rat. From 6 wk of age rats ate either ad libitum or 60% of the amount consumed by those eating ad libitum. Calorie restriction had no effect on MAP of rats 12-14 mo of age; the MAP for the ad libitum fed and calorie-restricted groups were 114.6 +/- 1.6 and 111.6 +/- 0.8 mmHg, respectively. Basal heart rate (HR), however, was reduced from 396 +/- 6 beats/min in the libitum-fed group to 333 +/- 5 beats/min in the calorie-restricted group. Administration of sodium nitroprusside (SNP) (both as bolus and constant infusion) and phenylephrine (PE) (bolus alone) elicited tachycardia and bradycardia in both groups. The calorie-restricted group exhibited greater baroreflex responsiveness to hypotensive stress than did the ad libitum-fed group. For constant infusion of SNP, the baroreflex gain of the calorie-restricted group (-5.43 +/- 0.56 beats.min-1.mmHg-1) was significantly greater than that of the ad libitum-fed group (-2.14 +/- 0.19 beats.min-1.mmHg-1). Bolus injections of SNP elicited similar results. Calorie restriction only minimally altered the baroreflex responsiveness to hypertensive stress elicited by bolus injections of PE, although the relationship between HR and MAP was shifted to the left in the calorie-restricted group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Ontogeny of baroreflex control of renal sympathetic nerve activity and heart rate.

The purpose of this study was to characterize the developmental changes in baroreflex function during fetal and postnatal life in sheep. Resting mean arterial blood pressure increased significantly from 55 +/- 2 mmHg in fetuses to 86 +/- 3 mmHg in newborn lambs and to 105 +/- 4 mmHg in 4- to 6-wk-old lambs. The sensitivity (gain) of the renal sympathetic nerve activity (RSNA) response to baroreceptor stimulation was greater (P < 0.05) in fetuses (-7.7 +/- 1.9%/mmHg) than in newborn (-2.9 +/- 0.1%/mmHg) and 4- to 6-wk-old lambs (-2.2 +/- 0.2%/mmHg). The threshold and saturation pressures for the baroreflex function curve were lower (P < 0.05) in fetuses (44 +/- 2 and 61 +/- 2 mmHg) than in newborn (59 +/- 4 and 106 +/- 5 mmHg) or 4- to 6-wk-old lambs (78 +/- 5 and 132 +/- 6 mmHg). Similar findings were observed when the heart rate response to baroreceptor stimulation was examined. Additional experiments were performed in newborn and 4- to 6-wk-old lambs to determine whether the rise in arterial blood pressure associated with postnatal maturation contributed to baroreflex resetting. Sustained elevation of arterial blood pressure by 15-20 mmHg for over 90 min did not reset the baroreflex function curve in either newborn or 4- to 6-wk-old lambs.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog.

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Animals↗
PubMed1986

Angiotensin II attenuates baroreflexes at nucleus tractus solitarius of rats.

Microinjection of angiotensin II (ANG II) into the nucleus tractus solitarius (NTS) has been shown to produce a dose-dependent increase in blood pressure and heart rate. We have tested the effect of subpressor infusions of ANG II (10 ng . kg-1 . min-1) in the NTS on reflex bradycardia after intravenous administration of the vasoconstrictor phenylephrine (1-12 micrograms) in normotensive urethan-anesthetized rats. ANG II within the brain is thought to contribute to the decreased baroreflex sensitivity in spontaneously hypertensive rats (SHR). The sensitivity of the baroreflex was significantly decreased by the infusion of ANG II (1.01 +/- 0.08) compared with control (2.41 +/- 0.51) in the normotensive animals. Baroreflex sensitivity was significantly decreased in SHR (0.40 +/- 0.21) compared with normotensive animals. We conclude that ANG II within the NTS can inhibit the function of baroreceptor reflexes in normotensive animals, suggesting that the endogenous peptide may perform an inhibitory role in the baroreflex arc, and this is further evidence that central ANG II is involved in blood pressure of SHR.

Angiotensin II↗
PubMed1990

Parasympathetic impairment of baroreflex control of heart rate in Dahl S rats.

To test the hypothesis that impaired baroreflex control of heart rate in Dahl salt-sensitive (S) rats is due to an impairment of the parasympathetic limb of the bradycardic response, baroreflex sensitivity was evaluated in conscious, chronically instrumented Dahl S and salt-resistant (R) animals. Sensitivity was impaired in Dahl S rats when bolus doses of phenylephrine were administered (0.863 +/- 0.042 vs. 1.43 +/- 0.055 ms/mmHg), but it was not different than in R rats when tested with sodium nitroprusside. When the sensitivities before and after blocking the parasympathetic nervous system with atropine were compared, it was revealed that 82% of the reflex bradycardia resulting from bolus doses of phenylephrine was due to the parasympathetic nervous system, whereas the majority (73%) of the bradycardia induced by 5-min infusions of phenylephrine was due to withdrawal of sympathetic tone. Neither baroreflex sensitivity to infusions of phenylephrine (73% sympathetic) or to infusions after atropine (100% sympathetic) were significantly different between S and R rats. Therefore, the impairment of the heart rate reflex in Dahl S rats is due to an impairment of the parasympathetic limb of the response. In addition, a high-salt diet before the development of hypertension did not alter baroreflex sensitivity in either Dahl S or R rats.

Animals↗
PubMed1991

Impairment of carotid-cardiac vagal baroreflex in wheelchair-dependent quadriplegics.

The incidence of orthostatic hypotension can increase after prolonged exposure to chair rest and bedrest and is associated with post-bed rest impairment of the carotid-cardiac baroreflex response. We therefore hypothesized that the hypotension observed in humans confined to wheelchairs may be manifested by a reduced baroreflex sensitivity. We compared baroreflex responses of 16 wheelchair-dependent (WCD) quadriplegics with those of 15 able-bodied subjects (ABS) matched for age, height, and weight. Beat-to-beat R-R intervals were measured during application of graded pressures from 40 to -65 mmHg using a neck chamber for noninvasive stimulation of the carotid baroreceptors. Changes of R-R intervals were plotted against carotid distending pressures. The maximum slope of the stimulus-response relationship was greater (P less than 0.0001) in ABS (6.1 +/- 0.6 ms/mmHg) than in WCD (2.6 +/- 0.4 ms/mmHg). The range of the R-R interval response, i.e., the capacity to buffer blood pressure changes, was only 138 +/- 19 ms in WCD compared with 253 +/- 19 ms in ABS (P less than 0.001). Mean sitting systolic-to-diastolic blood pressures in WCD (92/60 mmHg) were less (P less than 0.0001) than in ABS (120/77 mmHg), although there were no significant differences between groups in supine resting blood pressures. Chronic loss of stimulation to carotid baroreceptors by routine standing posture is associated with attenuated sensitivity and reduced buffer capacity of the arterial baroreflex and hypotension during sitting in WCD patients.

Adult↗
PubMed1993

Carotid baroreflex control during hemorrhage in conscious and anesthetized dogs.

The hypothesis was tested that carotid baroreflex gain is increased after 20% hemorrhage. The baroreceptor reflex responses to changes in carotid sinus pressure (CSP) were measured in control, 20% hemorrhage, and reinfusion conditions in three experimental groups: conscious intact (n = 7), anesthetized intact (n = 8), and anesthetized vagotomized (n = 8) dogs. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), stroke volume (SV), and calculated total peripheral resistance (TPR) responses to changes in CSP were measured. At any given CSP, MAP, CO, and SV all decreased significantly with the 20% hemorrhage, as reflected by a downward shift in the reflex characteristic curve with no change in overall reflex range or gain. In contrast, TPR and HR responses to CSP were not significantly altered by 20% hemorrhage; reflex curves and gains were comparable to control conditions. In the conscious intact dogs, the maximal reflex gain, Gmax, for the MAP response was -1.365 +/- 0.25, -1.298 +/- 0.33, and -1.324 +/- 0.25 in control, 20% hemorrhage, and reinfusion conditions, respectively, and was not significantly altered by hemorrhage. In the same group, the Gmax for the HR response was -1.792 +/- 0.65, -1.709 +/- 0.33, and -1.986 +/- 0.67 in control, 20% hemorrhage, and reinfusion conditions, respectively; baroreflex gain on HR was not increased with hemorrhage. Plasma arginine vasopressin (AVP), an increase in which has been proposed to augment baroreflex gain, increased from a control level of 0.98 +/- 0.27 to 9.66 +/- 2.67 pg/ml during 20% hemorrhage in the conscious intact dogs; despite the increase in plasma AVP during hemorrhage, augmentation of baroreflex gain was not observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Diminished baroreflex control of forearm vascular resistance in physically fit humans.

The stimulus-response characteristics of cardiopulmonary baroreflex control of forearm vascular resistance (FVR) were studied in five unfit [UF, maximal O2 consumption (VO2 max) = 38.5 ml X min-1 X kg-1] and six fit (F, VO2 max = 57.0 ml X min-1 X kg-1) subjects. We assessed the relationship between reflex stimulus, i.e., changes in central venous pressure (CVP) and response, i.e., FVR, during selective unloading of the cardiopulmonary mechanoreceptors with lower body negative pressure (0 to -20 mmHg). The linear relationship between FVR and CVP, the gain of this baroreflex, was significantly diminished in the F subjects, -2.42 +/- 0.57 U/mmHg, compared with the UF, -5.15 +/- 0.58 U/mmHg. Both groups, F and UF, had similar resting values for CVP and FVR; thus the diminished gain in F subjects was not simply an artifact resulting from a shift of the set point along the baroreflex stimulus-response curve. We also found a linear relationship between baroreflex gain and total blood volume (r = 0.59, P less than 0.05). We conclude that the gain of this vascular reflex is attenuated in trained individuals and is related to cardiovascular adaptations, such as an increased blood volume, associated with exercise training.

Blood Pressure↗
PubMed1987

Exercise training and the arterial baroreflex.

To test the hypothesis that endurance training would attenuate the carotid sinus baroreflex in rats, studies were undertaken with 25 nontrained (NT) and 22 trained (T) male Sprague-Dawley rats that were exercised for 11-14 wk. Maximal O2 consumption was significantly increased 10% after training. The left carotid sinus region was functionally isolated in anesthetized animals. Subsequently, static carotid sinus pressure was raised in 20-Torr increments from 95 Torr until a maximal response in systemic arterial pressure and regional blood flows was recorded. Compared with the NT group, baroreflex control of blood pressure and calculated regional resistance of the T animals was less responsive to changes in carotid sinus pressure. Resting blood pressure, heart rate, and changes in peripheral blood flow velocity were similar for the two groups. Peripheral sensitivity to phenylephrine-HCl and hexamethonium bromide were also similar in the T and NT groups. It was concluded that the arterial baroreflex control of blood pressure was attenuated by exercise training. These findings support the concept that the trained individual is at disadvantage during hypotensive episodes and that endurance training will attenuate the sympathetic component of the arterial baroreflex.

Animals↗
PubMed1987

Effects of high-frequency jet ventilation on arterial baroreflex regulation of heart rate.

Fifteen anesthetized mechanically ventilated patients recovering from multiple trauma were studied to compare the effects of high-frequency jet ventilation (HFJV) and continuous positive-pressure ventilation (CPPV) on arterial baroreflex regulation of heart rate. Systolic arterial pressure and right atrial pressure were measured using indwelling catheters. Electrocardiogram (ECG) and mean airway pressure were continuously monitored. Lung volumes were measured using two linear differential transformers mounted on thoracic and abdominal belts. Baroreflex testing was performed by sequential intravenous bolus injections of phenylephrine (200 micrograms) and nitroglycerin (200 micrograms) to raise or lower systolic arterial pressure by 20-30 Torr. Baroreflex regulation of heart rate was expressed as the slope of the regression line between R-R interval of the ECG and systolic arterial pressure. In each mode of ventilation the ventilatory settings were chosen to control mean airway pressure and arterial PCO2 (PaCO2). In HFJV a tidal volume of 159 +/- 61 ml was administered at a frequency of 320 +/- 104 breaths/min, whereas in CPPV a tidal volume of 702 +/- 201 ml was administered at a frequency of 13 +/- 2 breaths/min. Control values of systolic arterial pressure, R-R interval, mean pulmonary volume above apneic functional residual capacity, end-expiratory pulmonary volume, right atrial pressure, mean airway pressure, PaCO2, pH, PaO2, and temperature before injection of phenylephrine or nitroglycerin were comparable in HFJV and CPPV. Baroreflex regulation of heart rate after nitroglycerin injection was significantly higher in HFJV (4.1 +/- 2.8 ms/Torr) than in CPPV (1.96 +/- 1.23 ms/Torr).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Aortic baroreflex control of heart rate during hypertensive stimuli: effect of fitness.

We examined the aortic baroreflex control of heart rate (HR) in seven healthy young men of average fitness (AF) and seven of high fitness (HF). The fitness level was determined by maximal oxygen uptake (AF = 42.9 +/- 1.1, HF = 62.3 +/- 1.8 ml.kg-1.min-1). Aortic baroreflex control of HR was determined during a steady-state increase of mean arterial pressure (MAP; AF, +15.0 +/- 2.1 and HF, +18.3 +/- 0.8 mmHg) with phenylephrine (PE) infusion combined with positive neck pressure (NP; AF, 18 +/- 2.0 and HF, 20 +/- 0.8 mmHg) to counteract the increased carotid sinus pressure and with low levels of lower body negative pressure to counteract the increased central venous pressure. There was no group difference in the increased MAP or NP, nor was there stage difference in MAP within either group during PE infusion. However, the isolated cardiac-aortic baroreflex gains (i.e., delta HR/delta MAP) were significantly less in the HF (0.16 +/- 0.02 and 0.14 +/- 0.03 beats.min-1.mmHg-1) than in the AF (0.52 +/- 0.08 and 0.59 +/- 0.07 beats.min-1.mmHg-1) subjects at PE + NP and PE + NP + lower body negative pressure. We concluded that during steady-state increases in MAP, the sensitivity of aortic baroreflex control of HR was significantly less in the HF than in the AF subjects.

Adolescent↗
PubMed1982

Comparison of techniques for measuring baroreflex sensitivity in man.

Because discrepancies about baroreflex sensitivity in essential hypertension may have resulted from the use of different measurement techniques, we assessed the extent to which the results of different techniques agree in the same subjects. The eight techniques studied were the change in RR interval per unit change in systolic pressure during the Valsalva maneuver, upon release of the Valsalva maneuver, after injection of phenylephrine and after injection of nitroglycerin; the changes in RR interval and in systolic pressure per mm Hg externally applied neck suction; and the changes in RR interval and systolic pressure per mm Hg externally applied neck pressure. The average intercorrelation among these measures in 30 subjects was statistically significant (r = 0.36, p less than 0.01), but suggests that variance in one measure accounted for an average of about 13% of the variance in other measures. Standard deviations among subjects were often as large as the mean, indicating important interindividual variability as well. These findings demonstrate that baroreflex sensitivity varies widely among subjects and that different techniques for measuring baroreflex sensitivity probably measure different aspects of baroreflex function.

Adult↗
PubMed1989

Nifedipine potentiates cardiopulmonary baroreflex control of sympathetic nerve activity in healthy humans. Direct evidence from microneurographic studies.

Nifedipine augments baroreflex mechanisms in in vivo animal models. Previous studies in our laboratory demonstrate that nifedipine potentiates baroreflex control of heart rate and vascular resistance in normal human subjects. To further define the neuroeffector mechanism of the autonomic effects of nifedipine, we directly measured postganglionic sympathetic nerve activity to muscle (MSNA, microneurography), before and after drug administration, during selective unloading of cardiopulmonary baroreceptors with lower body negative pressure (-10 mm Hg, LBNP-10), and during the cold pressor test. Twenty-three normal subjects (age, 23 +/- 1 years; mean +/- SEM) were studied in the control state and 20 minutes after administration of either nifedipine (10 mg s.l., 10 subjects), during nitroprusside infusion (0.37 +/- 0.03 microgram/kg/min i.v., eight subjects), or 20 minutes after sublingual administration of placebo (five subjects). We measured systemic arterial pressure, central venous pressure, heart rate, and MSNA. Nifedipine and nitroprusside produced similar increases in resting heart rate and MSNA and similar decreases in central venous pressure, whereas placebo had no effect on resting hemodynamics. During LBNP-10, hemodynamic changes were not significantly different among the three treatment groups. However, the percentage increase in MSNA during LBNP-10 was significantly augmented from a 24 +/- 9% increase before nifedipine to a 56 +/- 7% increase after nifedipine (p less than 0.05). Decreases in central venous pressure with LBNP-10 were nearly identical before compared with after nifedipine. Thus, nifedipine increased the cardiopulmonary baroreflex sympathetic sensitivity (change in total MSNA per mm Hg decrease in central venous pressure during LBNP-10) from 26.5 +/- 10.7 units/mm Hg to 74.9 +/- 19.0 units/mm Hg (p less than 0.01). In contrast, administration of hemodynamically similar doses of nitroprusside resulted in an attenuation of MSNA responses to LBNP-10. During LBNP-10, MSNA increased 57 +/- 12% before nitroprusside but only 14 +/- 4% during nitroprusside (p less than 0.01). The cardiopulmonary baroreflex sympathetic sensitivity was not significantly altered by nitroprusside (45.1 +/- 12.4 units/mm Hg before compared with 33.1 +/- 20.8 units/mm Hg during nitroprusside, p = NS). Placebo had no effect on the responses to LBNP-10. Nifedipine did not augment MSNA responses to the cold pressor test. To evaluate the linearity of sympathetic responses to cardiopulmonary baroreceptor unloading, graded LBNP (0, -5, -10, and -15 mm Hg) was applied in three additional subjects before and after nifedipine (10 mg s.l.).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1998

Voltage-dependent calcium channel promoter restores baroreflex sensitivity in conscious dogs with heart failure.

BACKGROUND: The aim of this study was to determine the mechanism by which the calcium channel promoter BAY y 5959 affects the control of heart rate and baroreflex sensitivity in conscious dogs with pacing-induced heart failure (HF). METHODS AND RESULTS: We compared responses to BAY y 5959, which increases inotropy and decreases chronotropy, with those to norepinephrine (NE), which coincidentally exerts the same directional effects on inotropy and chronotropy, albeit through different mechanisms, in the presence and absence of ganglionic blockade both in control and in HF. Both BAY y 5959 and NE elicit direct effects on the heart and indirect effects through activation of reflexes, primarily the sinoaortic baroreceptor reflex. BAY y 5959 still reduced heart rate in dogs with arterial baroreceptor denervation, but not after ganglionic blockade. HF induced classic catecholamine desensitization to the inotropic effects of NE and blunted reflex bradycardia. In contrast, inotropic responses to BAY y 5959 were preserved in HF. Surprisingly, the autonomically mediated bradycardia induced by BAY y 5959 was also preserved in HF. Baroreflex sensitivity was assessed in control and in HF by pulse interval-systolic arterial blood pressure (PI/SAP) slopes constructed in response to pharmacological alterations in arterial pressure. HF depressed the PI/SAP slope from 11.5+/-1.3 to 4.8+/-0.9 ms/mm Hg, but during BAY y 5959 infusion in HF, the PI/SAP slope was restored to 24.1+/-5.2 ms/mm Hg. To assess central versus peripheral actions of BAY y 5959, the agent was infused with intra-carotid artery perfusion at a low dose, which acted centrally but did not have an effect peripherally. Under these conditions, it still decreased heart rate and restored baroreflex sensitivity (PI/SAP slope, 12.7+/-2.8 ms/mm Hg). CONCLUSIONS: Thus, the calcium promoter restores arterial baroreflex sensitivity in HF. Based on intra-carotid artery experiments, this occurs through a central nervous system and vagal mechanism.

Animals↗
PubMedDate not supplied

Central effect of intravenous phenylephrine on baroreflex control of renal nerves.

Responses of renal sympathetic nerve activity were determined in eight chloralose-anesthetized rabbits during sustained (1-3 minutes) increases in arterial pressure induced by phenylephrine infusion, and as arterial pressure returned to control. In four of the eight experiments, aortic baroreceptor traffic was also recorded. When arterial pressure was raised from 81 +/- 5 to 110 +/- 7 mm Hg, renal nerve activity decreased from 30 +/- 7 to 1 +/- 1 imp/sec. Aortic nerve activity increased from 208 +/- 35 to 346 +/- 49 imp/sec. When pressure returned to control (81 +/- 5 mm Hg), renal nerve activity remained inhibited (7 +/- 2 imp/sec), even though aortic nerve activity had also returned to control (195 +/- 33 imp/sec). Arterial pressure and traffic in the renal and aortic nerves returned to control over the succeeding 1 to 5 minutes. Transient increases in arterial pressure (lasting less than 1 minute) due to bolus injections of phenylephrine resulted in inhibition of renal nerve traffic followed by rapid recovery. In five rabbits with aortic and vagal nerves sectioned and both carotid sinuses isolated from the circulation, intravenous phenylephrine infusion augmented the gain of the isolated carotid baroreflex (particularly at low carotid sinus pressures). In nine experiments, injection of phenylephrine (0.01, 0.1, or 1.0 microgram) into the lateral ventricles did not change the basal renal nerve traffic but augmented the gain of the baroreflex control of the renal nerves. Our data indicate that peripherally infused phenylephrine can alter the arterial baroreflex control of the renal nerves by a central effect. The similar influence of intracerebroventricular phenylephrine on baroreflex control of the renal nerves is consistent with this view.

Animals↗
PubMed1986

Arterial baroreflexes and blood pressure and heart rate variabilities in humans.

The factors responsible for 24-hour blood pressure and heart rate variabilities have never been clarified; however, studies performed in unanesthetized animals have shown an increase in blood pressure variability after sinoaortic denervation, and a negative relationship has been reported occasionally between blood pressure variability and baroreflex control of heart rate in humans. We have systematically investigated this issue in 82 ambulant hypertensive subjects using 24-hour intraarterial blood pressure recording (Oxford method) in which blood pressure and heart rate variabilities were measured by calculating the standard deviations of the values obtained throughout the 24 hours or during separate daytime and nighttime periods. Baroreflex sensitivity was assessed by the bradycardic or tachycardic responses to intravenous injections of phenylephrine or nitroglycerin and by the blood pressure response to changes in carotid transmural pressure obtained with a neck chamber. The sensitivity of the baroreceptor-heart rate reflex as assessed by the vasoactive drug technique showed a negative relationship with 24-hour blood pressure variability as well as with daytime and nighttime blood pressure variabilities measured separately (r = -0.28 to -0.50, p less than 0.05). These variabilities also correlated negatively with the sensitivity of the baroreceptor-blood pressure reflex as assessed by the neck chamber technique. By contrast, baroreflex sensitivity showed a positive correlation with heart rate variabilities (r = 0.32 to 0.47, p less than 0.05). The relationship between baroreflex sensitivity and blood pressure and heart rate variabilities was confirmed when the data were analyzed by multiple regression to adjust for blood pressure and age differences among the 82 subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

High salt diet sensitizes cardiopulmonary baroreflexes in Dahl salt-resistant rats.

Compared with Dahl salt-resistant (R) rats, Dahl salt-sensitive (S) rats on a low salt diet have impaired cardiopulmonary baroreflex control of sympathetic nerve activity. The purpose of this study was to examine the sensitivity of cardiopulmonary baroreflex function in both strains of Dahl rats when they are challenged with a high salt diet. We studied Dahl R and S rats after 6 weeks of low and high salt diets. To assess cardiopulmonary baroreflex function, we measured decreases in splanchnic sympathetic nerve activity produced by increases in left ventricular end-diastolic pressure during graded volume expansion (dextran 75) after bilateral sinoaortic denervation. A given amount of infused volume produced comparable increases in left ventricular end-diastolic pressure in Dahl R rats on low and high salt diets but significantly greater decreases in sympathetic nerve activity in the high salt group than in the low salt group. Thus, the high salt diet augmented the sympathoinhibitory response to volume expansion in the Dahl R rats. In contrast, among the Dahl S rats equivalent increases in left ventricular end-diastolic pressure during volume expansion produced smaller sympathoinhibitory responses in the high salt group than in the low salt group. The gain of the cardiopulmonary baroreflex, expressed as the percentage decrease in sympathetic nerve activity per mm Hg increase in left ventricular end-diastolic pressure, was significantly increased by a high salt diet in Dahl R rats but tended to be decreased by a high salt diet in Dahl S rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Relative contributions of cardiopulmonary and sinoaortic baroreflexes in causing sympathetic activation in the human skeletal muscle circulation during orthostatic stress.

The aim of this study was to reexamine the hypothesis that cardiopulmonary baroreflexes are more important than sinoaortic baroreflexes in causing vasoconstriction in the skeletal muscle circulation during orthostatic stress. We recorded muscle sympathetic nerve activity (MSNA) with microelectrodes in the peroneal nerve (and forearm blood flow with venous occlusion plethysmography) in normal subjects (innervated ventricles) and in heart transplant recipients (denervated ventricles) during graded lower body negative pressure (LBNP) performed alone and in combination with intravenous infusion of phenylephrine, which was titrated to eliminate the orthostatically induced fall in blood pressure and thus the unloading of both carotid and aortic baroreceptors. The principal new findings are as follows: (1) The increases in both MSNA and forearm vascular resistance during multiple levels of LBNP were not attenuated by heart transplantation, which causes ventricular but not sinoaortic deafferentation. (2) In heart transplant recipients, a small increase in MSNA during mild LBNP was dependent on a decrease in arterial pressure, but in normal subjects, a similar increase in MSNA occurred in the absence of any detectable decrease in the aortic pressure stimulus to the sinoaortic baroreceptors. (3) In normal subjects, the large increase in MSNA during a high level of LBNP was dependent on a decrease in arterial pressure and could be dissociated from the decrease in central venous pressure. Taken together, the findings strongly suggest that sinoaortic baroreflexes are much more important and ventricular baroreflexes are much less important than previously thought in causing reflex sympathetic activation and vasoconstriction in the human skeletal muscle circulation during orthostatic stress.

Female↗