Baroreflex Control Of Sympathetic Activity Research Articles

Attenuated Sympathetic Baroreflex Sensitivity Evoked by Acute Mental Stress but not Prolonged Sleep Restriction in Healthy Adults

BackgroundPsychological stress and insufficient sleep are both associated with an increased risk of developing hypertension. While the underlying mechanisms are not well defined, it has been postulated that this may be facilitated by modulation of baroreflex control of sympathetic activity. Short periods (<5 min) of mental stress attenuate sympathetic baroreflex sensitivity (sBRS), but it is currently unclear whether this holds true for longer bouts of stress. As such, we sought to examine the effect of 10 min of mental stress on sBRS. Additionally, we evaluated the impact of experimental sleep restriction on baroreflex control of blood pressure during mental stress. We hypothesized that mental stress would attenuate sBRS, and that prolonged exposure to restricted sleep would result in a greater reduction in sBRS during mental stress.MethodsFourteen healthy adults (10M/4F, 25±1 yrs) underwent 10 min of mental stress consisting of a 5‐min mental arithmetic task, followed immediately by a 5‐min Stroop color‐word conflict test. Heart rate (electrocardiography), blood pressure (finger photoplethysmography), and muscle sympathetic nerve activity (microneurography of the common peroneal nerve) were continuously measured to determine sBRS at baseline and during mental stress. A subset of participants (n=9) completed the mental stress protocol under both experimental sleep restriction (4 hr/night) and control sleep conditions (8–9 hr/night) while inpatient at a hospital‐based clinical research unit. Subjects underwent a 3‐night acclimation period, followed by 9 or 14 nights of either sleep restriction or control sleep. Data from Day 2/1 or Day 13/15 (during control sleep only) were used to assess the effect of mental stress alone, and data from Day 13/15 (under both conditions) were used to assess the effect of sleep restriction.ResultsAcute mental stress resulted in a marked blunting of sBRS from baseline (−2.7±0.5 to −1.5±0.4 bursts·100hb−1·mmHg−1, p=0.04). Examining the mental stress interventions individually revealed a significant decrease in sBRS during the initial 5 min of stress (mental arithmetic, p=0.03), but not during the subsequent 5 min of testing (Stroop test, p=0.75). Mental stress also reduced baroreflex function following sleep restriction (main effect of condition, p<0.01); however, the reduction in sBRS was not significantly different in restricted sleep compared to control (main effect of visit, p=0.78). There was no significant interaction effect between sleep restriction and mental stress (p=0.81).ConclusionsThese data provide further support that, in young healthy individuals, sBRS is attenuated early in mental stress but quickly returns to baseline values. In contrast, prolonged sleep restriction does not appear to alter sympathetic control of blood pressure.Support or Funding InformationNIH HL114024 (VKS), NIH HL114676 (VKS), NIH HL083947 (MJJ), FAER Medical Student Anesthesia Research Fellowship (NMP)

Baroreflex control of renal sympathetic nerve activity in early heart failure assessed by the sequence method.

The integrity of the baroreflex control of sympathetic activity in heart failure (HF) remains under debate. We proposed the use of the sequence method to assess the baroreflex control of renal sympathetic nerve activity (RSNA). The sequence method assesses the spontaneous arterial pressure (AP) fluctuations and their related changes in heart rate (or other efferent responses), providing the sensitivity and the effectiveness of the baroreflex. Effectiveness refers to the fraction of spontaneous AP changes that elicits baroreflex-mediated variations in the efferent response. Using three different approaches, we showed that the baroreflex sensitivity between AP and RSNA is not altered in early HF rats. However, the sequence method provided evidence that the effectiveness of baroreflex in changing RSNA in response to AP changes is markedly decreased in HF. The results help us better understand the baroreflex control of the sympathetic nerve activity. In heart failure (HF), the reflex control of the heart rate is known to be markedly impaired; however, the baroreceptor control of the sympathetic drive remains under debate. Applying the sequence method to a series of arterial pressure (AP) and renal sympathetic nerve activity (RSNA), we demonstrated a clear dysfunction in the baroreflex control of sympathetic activity in rats with early HF. We analysed the baroreflex control of the sympathetic drive using three different approaches: AP vs. RSNA curve, cross-spectral analysis and sequence method between AP and RSNA. The sequence method also provides the baroreflex effectiveness index (BEI), which represents the percentage of AP ramps that actually produce a reflex response. The methods were applied to control rats and rats with HF induced by myocardial infarction. None of the methods employed to assess the sympathetic baroreflex gain were able to detect any differences between the control and the HF group. However, rats with HF exhibited a lower BEI compared to the controls. Moreover, an optimum delay of 1 beat was observed, i.e. 1 beat is required for the RSNA to respond after AP changing, which corroborates with the findings related to the timing between these two variables. For delay 1, the BEI of the controls was 0.45±0.03, whereas the BEI of rats with HF was 0.29±0.09 (P<0.05). These data demonstrate that while the gain of the baroreflex is not affected in early HF, its effectiveness is markedly decreased. The analysis of the spontaneous changes in AP and RSNA using the sequence method provides novel insights into arterial baroreceptor reflex function.

Direct Evidences for Sympathetic Hyperactivity and Baroreflex Impairment in Tako Tsubo Cardiopathy

BackgroundThe exact pathophysiology of Tako-Tsubo cardiomyopathy (TTC) remains unknown but a role for sympathetic hyperactivity has been suggested. Up to now, no direct evidence of sympathetic nerve hyperactivity has been established nor involvement of sympathetic baroreflex identified. The aim of our study was to determine, by direct sympathetic nerve activity (SNS) recording if sympathetic nervous system activity is increased and spontaneous baroreflex control of sympathetic activity reduced in patients with TTC.MethodsWe included 13 patients who presented with TTC and compared their SNS activity and spontaneous baroreflex control of sympathetic activity with that of 13 control patients with acutely decompensated chronic heart failure. SNS activity was evaluated by microneurography, a technique assessing muscle sympathetic nerve activity (MSNA). Spontaneous baroreflex control of sympathetic activity was evaluated as the absolute value of the slope of the regression line representing the relationship between spontaneous diastolic blood pressure values and concomitant SNS activity. Control patients were matched for age, sex, left ventricular ejection fraction and creatinine clearance.ResultsThe mean age of the patients with TTC was 80 years, all patients were women. There were no significant differences between the two groups of patients for blood pressure, heart rate or oxygen saturation level. TTC patients presented a significant increase in sympathetic nerve activity (MSNA median 63.3 bursts/min [interquartile range 61.3 to 66.0] vs median 55.7 bursts/min [interquartile range 51.0 to 61.7]; p = 0.0089) and a decrease in spontaneous baroreflex control of sympathetic activity compared to matched control patients (spontaneous baroreflex control of sympathetic activity median 0.7%burst/mmHg [interquartile range 0.4 to 1.9] vs median 2.4%burst/mmHg [interquartile range 1.8 to 2.9]; p = 0.005).ConclusionsWe report for the first time, through direct measurement of sympathetic nerve activity, that patients with TTC exhibit elevated SNS activity associated with a decrease in spontaneous baroreflex control of sympathetic activity. These data may explain the pathophysiology and clinical presentation of patient with TTC.

Reduction of superoxide in the nucleus of solitary tract improves baroreflex control of sympathetic activity in chronic heart failure rats

Reduction of superoxide in the nucleus of solitary tract improves baroreflex control of sympathetic activity in chronic heart failure rats

ANGIOTENSIN‐(1‐7) ICV CHRONIC INFUSION IMPROVES BAROREFLEX CONTROL OF RENAL SYMPATHETIC NERVE ACTIVITY IN DOCA‐SALT HYPERTENSIVE RATS

We evaluated the effect of angiotensin‐(1‐7) [Ang‐(1‐7)] ICV chronic infusion in baseline and baroreflex control of renal sympathetic nerve activity (RSNA) in DOCA‐salt hypertensive rats. Sprague‐Dawley rats were submitted to uninephrectomy (UNX) or DOCA‐salt hypertension model (UNX + DOCA + saline). After 7 days, Ang‐(1‐7) ICV infusion (0.2 nmol/ 0.5 μl/ hour) or 0.9% sterile saline (0.5 μl/ hour) was initiated by osmotic mini‐pumps for 14 days. On the 21th day, the animals were anaesthetized (urethane; i.p.) and baseline arterial pressure (MAP), heart rate (HR) and RSNA, and baroreflex control RSNA were evaluated. As expected, DOCA‐salt treatment induced an increase in baseline MAP (122 ± 3 mmHg, n=4 vs 93 ± 2 mmHg, n=5, UNX), reduced baroreflex control of RSNA (1.33 ± 0.10 %ΔRSNA/ mmHg, n=4 vs 2.73 ± 0.29 %ΔRSNA/ mmHg, n=5, UNX), without any changes in baseline HR or RSNA (130 ± 17 spikes/sec, n=5 vs 118 ± 12 spikes/sec, n=4 UNX). Animals submitted to Ang‐(1‐7) ICV infusion presented a reduced MAP (conscious rats) and a greater baroreflex control of RSNA (2.24 ± 0.20 %ΔRSNA/ mmHg, n=4), without any significant in baseline RSNA (113 ± 10 spikes/sec, n=4). These results showed that central Ang‐(1‐7) modulates baroreflex control of RSNA in DOCA‐salt rats, and suggest that chronic increase in Ang‐(1‐7) levels in the brain may attenuate high blood pressure, in part by improving baroreflex control of sympathetic activity.

Is baroreflex control of sympathetic activity and heart rate active in the preterm fetal sheep?

The arterial baroreflex is a fundamental reflex that buffers rapid changes in arterial blood pressure (BP) via regulation of the heart rate and sympathetic nerve activity to the vasculature. In adults a sigmoidal relationship between BP and both heart rate and sympathetic nerve activity is well documented. Its role in blood pressure control before birth is unclear. Preterm babies have a high incidence of low BP, especially in the first few days of life, which could be related, in part, to immaturity of the baroreflex. In the present study, we investigated the baroreflex control of fetal heart rate and renal sympathetic nerve activity (RSNA) in preterm fetal sheep in utero (102 +/- 1 days of gestation; term 140 days). Phenylephrine was associated with a significant increase in BP from 38 +/- 2 to 58 +/- 3 mmHg and a decrease in heart rate (HR) from 177 +/- 4 to 116 +/- 8 beats per minute (bpm). Sodium nitroprusside was associated with a significant fall in BP from 38 +/- 2 to 26 +/- 1 mmHg and an increase in HR from 182 +/- 4 to 274 +/- 8 bpm. However, the time between the 50% changes in BP and HR was significantly greater after hypotension than hypertension (31 +/- 8 s vs. 14 +/- 5 s, P < 0.05). No significant changes in RSNA occurred with either stimulus. This suggests that there are different maturational tempos for the components of the central autonomic response to altered blood pressure.

Impaired baroreflex sensitivity as a potential marker of cardiovascular risk in hypertension

Impaired baroreflex sensitivity as a potential marker of cardiovascular risk in hypertension

Influence of plasma osmolality on baroreflex control of sympathetic activity

The purpose of this study was to determine if plasma osmolality alters baroreflex control of sympathetic activity when controlling for a change in intravascular volume; we hypothesized that baroreflex control of sympathetic activity would be greater during a hyperosmotic stimulus compared with an isoosmotic stimulus when intravascular volume expansion was matched. Seven healthy subjects (25 +/- 2 yr) completed two intravenous infusions: a hypertonic saline infusion (HSI; 3% NaCl) and, on a separate occasion, an isotonic saline infusion (ISO; 0.9% NaCl), both at a rate of 0.15 ml x kg(-1) x min(-1). To isolate the effect of osmolality, comparisons between HSI and ISO conditions were retrospectively matched based on hematocrit; therefore, baroreflex control of sympathetic outflow was determined at 20 min of a HSI and 40 min of an ISO. Muscle sympathetic outflow (MSNA) was directly measured using the technique of peroneal microneurography; osmolality and blood pressure (Finometer) were assessed. The baroreflex control of sympathetic outflow was estimated by calculating the slope of the relationship between MSNA and diastolic blood pressure during controlled breathing. Plasma osmolality was greater during the HSI compared with the ISO (HSI: 292 +/- 0.9 mosmol/kg and ISO: 289 +/- 0.8 mosmol/kg, P < 0.05). Hematocrits were matched (HSI: 39.1 +/- 1% and ISO: 39.1 +/- 1%, P > 0.40); thus, we were successful in isolating osmolality. The baroreflex control of sympathetic outflow was greater during the HSI compared with the ISO (HSI: -8.3 +/- 1.2 arbitrary units x beat(-1) x mmHg(-1) vs. ISO: -4.0 +/- 0.8 arbitrary units x beat(-1) x mmHg(-1), P = 0.01). In conclusion, when controlling for intravascular volume, increased plasma osmolality enhances baroreflex control of sympathetic activity in humans.

Baroreflex Control of Sympathetic Activity

Various experimental models have been used to establish a link between plasma osmolality and sympathetic activity. However, in humans, it is difficult to experimentally isolate the contribution of plasma osmolality to the baroreflex control of sympathetic activity due to the varying changes in plasma volume (P V): with a dehydration model, there is a decrease in PV and an increase in osmolality; with a salt loading model, there is an increase in PV and an increase in osmolality. PURPOSE: To determine if plasma osmolality (for a given change in PV) alters baroreflex control of sympathetic activity; we hypothesized that baroreflex control of sympathetic activity would be greater during an osmotic stimulus compared to a volume-matched stimulus. METHODS: Seven healthy subjects (25±2yrs) completed 2 intravenous infusions: a hypertonic saline infusion (HSI: 3% NaCl) and on a separate occasion, an isotonic saline infusion (ISO: 0.9% NaCl), both at a rate of 0.15 ml/kg/min. In order to isolate the effect of osmolality, comparisons between the HSI and ISO conditions were retrospectively matched based on hematocrit (Hct); therefore, baroreflex control of sympathetic outflow (SBRS) was determined at 20 minutes of the HSI and 40 minutes of the ISO. Muscle sympathetic outflow (MSNA) was directly measured using the technique of peroneal microneurography. MSNA, osmolality, and blood pressure (Finometer; BP) were assessed. SBRS was determined by calculating the slope of the relationship between MSNA and diastolic BP during controlled breathing. A one-way repeated measures ANOVA and post-hoc tests (when appropriate) were used for statistical analysis (the alpha level was set at p<0.05). RESULTS: (mean ± SE): Plasma osmolality was greater during the HSI compared to ISO (HSI: 292±1, ISO: 289±1 mOsmols/kg; p<0.05). Hcts were matched (HSI: 39.1±1, ISO: 39.1±1%; p>0.40); thus we were successful in isolating osmolality. SBRS was greater during the HSI compared to the ISO (HSI: −8.3±1.2vs. ISO: −4.0±0.8 au/beat/mmHg; p=0.018). CONCLUSIONS: Increased plasma osmolality enhances baroreflex control of sympathetic activity in humans. The interaction between plasma osmolality and sympathetic outflow may be an important neural mechanism contributing to cardiovascular control. Supported by NIH grant R15 HL074851–01

Heart rate turbulence parameters correlate with post–premature ventricular contraction changes in muscle sympathetic activity

Heart rate turbulence (HRT) has been shown to be vagally mediated with a strong correlation to baroreflex indices. However, the relationship between HRT and peripheral sympathetic nerve activity (SNA) after a premature ventricular contraction (PVC) remains unclear. We sought to evaluate the relationship between HRT and the changes in peripheral SNA after PVCs. We recorded postganglionic muscle SNA during electrocardiogram monitoring in eight patients with spontaneous PVCs. Fifty-two PVCs were observed and analyzed for turbulence onset (TO) and slope (TS). SNA was quantified during (1) the dominant burst after the PVC (dominant burst area) and (2) the 10 seconds after the dominant burst (postburst SNA). The mean TO was 0.1% +/- 4.6%, and the mean TS was 6.1 +/- 6.6. The dominant burst area negatively correlated with TO (r = -0.50, P = .0002). The postburst SNA showed a significant positive correlation with TO (r = 0.44, P = .001) and a negative correlation with TS (r = -0.42, P = .002). These correlations remained significant after controlling for either the PVC coupling interval or the left ventricular ejection fraction. Our findings highlight the relationship between perturbations in HRT and pathology in the sympathetic limb of the autonomic nervous system. Future studies are needed to evaluate the prognostic role of baroreflex control of sympathetic activity in patients with structural heart disease.

Baroreflex resetting during exercise: mechanisms and meaning

the cardiovascular adjustments to exercise constitute well- coordinated responses throughout the body. Virtually every organ system is required to do more (e.g., skeletal muscle, the respiratory pump, and the cardiac pump) or to do the same as at rest while receiving less blood flow. Of all the

Balance between cardiac output and sympathetic nerve activity in resting humans: role in arterial pressure regulation

Large, reproducible interindividual differences exist in resting sympathetic nerve activity among normotensive humans with similar arterial pressures, resulting in a lack of correlation between muscle sympathetic nerve activity (MSNA) and arterial pressure among individuals. Although it is known that the arterial pressure is the main short-term determinant of MSNA in humans via the arterial baroreflex, the lack of correlation among individuals suggests that the level of arterial pressure is not the only important input in regulation of MSNA in humans. We studied the relationship between cardiac output (CO) and baroreflex control of sympathetic activity by measuring MSNA (peroneal microneurography), arterial pressure (arterial catheter), CO (acetylene uptake technique) and heart rate (HR; electrocardiogram) in 17 healthy young men during 20 min of supine rest. Across individuals, MSNA did not correlate with mean or diastolic blood pressure (r<0.01 for both), but displayed a significant negative correlation with CO (r=-0.71, P=0.001). To assess whether CO is related to arterial baroreflex control of MSNA, we constructed a baroreflex threshold diagram for each individual by plotting the percentage occurrence of a sympathetic burst against diastolic pressure. The mid-point of the diagram (T50) at which 50% of cardiac cycles are associated with bursts, was inversely related to CO (r=-0.75, P<0.001) and stroke volume (SV) (r=-0.57, P=0.015). We conclude that dynamic inputs from CO and SV are important in regulation of baroreflex control of MSNA in healthy, normotensive humans. This results in a balance between CO and sympathetically mediated vasoconstriction that may contribute importantly to normal regulation of arterial pressure in humans.

Effects of 17beta-estradiol on the baroreflex control of sympathetic activity in conscious ovariectomized rats.

The effects of chronic treatment with 17beta-estradiol on baroreflex control of sympathetic activity were examined in conscious unrestrained ovariectomized rats. Baroreflex function was evaluated by logistic sigmoidal analysis of the relationships between changes in mean arterial pressure (MABP) and changes in heart rate (HR) and splanchnic nerve activity (SNA) when MABP was rapidly increased to 150 mmHg by intravenous phenylephrine after its reduction to 50 mmHg by intravenous nitroprusside. These baroreflex function curves were similar in vehicle- and estradiol-treated rats. However, after a 30-min infusion of vasopressin in vehicle-treated rats, the curve for HR was shifted downward, and the upper plateau and maximum gain for the SNA curve were reduced. These effects were abolished by estradiol. A 30-min phenylephrine infusion had no effect on the baroreflex curves. Thus estrogen can modulate the action of vasopressin on baroreflex control of sympathetic outflow and thereby participate in cardiovascular regulation.

Baroreflex control of sympathetic activity in experimental hypertension.

The arterial baroreceptor reflex system is one of the most powerful and rapidly acting mechanisms for controlling arterial pressure. The purpose of the present review is to discuss data relating sympathetic activity to the baroreflex control of arterial pressure in two different experimental models: neurogenic hypertension by sinoaortic denervation (SAD) and high-renin hypertension by total aortic ligation between the renal arteries in the rat. SAD depresses baroreflex regulation of renal sympathetic activity in both the acute and chronic phases. However, increased sympathetic activity (100%) was found only in the acute phase of sinoaortic denervation. In the chronic phase of SAD average discharge normalized but the pattern of discharges was different from that found in controls. High-renin hypertensive rats showed overactivity of the renin angiotensin system and a great depression of the baroreflexes, comparable to the depression observed in chronic sinoaortic denervated rats. However, there were no differences in the average tonic sympathetic activity or changes in the pattern of discharges in high-renin rats. We suggest that the difference in the pattern of discharges may contribute to the increase in arterial pressure lability observed in chronic sinoaortic denervated rats.

Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure

Objectives. This study sought to determine the effects of enalaprilat on reflex control of sympathetic nerve activity.Background. Angiotensin-converting enzyme inhibitors decrease mortality in patients with congestive heart failure. Their efficacy appears to be related importantly to antiadrenergic effects, the mechanism for which has not been determined. Because baroreflexes tonically inhibit sympathetic outflow, and baroreflexes are blunted in heart failure, we hypothesized that these agents reduce sympathetic activity by augmenting baroreflexes.Methods. We assessed baroreflex control sympathetic nerve activity and heart rate in patients with congestive heart failure and in control subjects before and after enalaprilat (0.02 mg/kg body weight intravenously). Arterial baroreflexes were perturbed by bolus administration of sodium nitroprusside and phenylephrine. Cardiopulmonary baroreflexes were perturbed by lower body negative pressure and head-down tilt. Muscle sympathetic nerve activity was recorded by microneurography.Results. Enalaprilat decreased systolic blood pressure in patients with heart failure and control subjects. Sympathetic nerve activity increased in control subjects but decreased in patients with heart failure after enalaprilat despite reductions in central venous pressure in this group. Baroreflex control of sympathetic nerve activity was unchanged by enalaprilat in control subjects. In patients with heart failure, both arterial and cardiopulmonary baroreflex control of sympathetic nerve activity was enhanced by enalaprilat. Baroreflex control of heart rate was unchanged by enalaprilat in either group.Conclusions. Enalaprilat augments both arterial and cardiopulmonary baroreflex control of sympathetic activity in heart failure. These augmented inhibitory influences are associated with a reduction in sympathetic outflow and may contribute to the beneficial effects of angiotensin-converting enzyme inhibitors in heart failure.

Contrasting effects of digitalis and dobutamine on baroreflex sympathetic control in normal humans.

Digitalis glycosides augment cardiopulmonary baroreceptor mechanisms in animals. This could result from inotropic actions or from direct sensitization of cardiac mechanoreceptors. To determine if digitalis has similar actions in humans and to evaluate the mechanisms involved, we measured muscle sympathetic nerve activity (MSNA; microneurography) during unloading of cardiopulmonary baroreceptors with incremental lower body negative pressure (LBNP; 0 to -15 mm Hg) and during the cold pressor test in 22 normal subjects (age 22 +/- 1 year, mean +/- SEM). Arterial and central venous pressures, heart rate, and MSNA were measured during LBNP before and after intravenous digitalis (Cedilanid 0.02 ng/kg, n = 8), dobutamine (2.8 +/- 0.5 micrograms/kg/min, n = 8), or placebo (n = 6). Digitalis and dobutamine produced similar increases in baseline mean arterial pressure and decreases in central venous pressure and MSNA. LBNP produced similar decreases in central venous pressure in all groups before and after drug administration. The MSNA responses to LBNP were markedly potentiated by digitalis but not by dobutamine or placebo. Digitalis did not alter responses to the cold pressor test. Thus, digitalis selectively potentiated cardiopulmonary baroreflex regulation of sympathetic neural responses in normal humans, whereas dobutamine (another positive inotropic agent) did not produce this effect. We conclude that digitalis augments cardiopulmonary baroreflex control of sympathetic activity, probably by direct baroreceptor sensitization.

Sympathetic nerve rhythm of brain stem origin.

ARTICLESSympathetic nerve rhythm of brain stem originS. M. Barman, and G. L. GebberS. M. Barman, and G. L. GebberPublished Online:01 Jul 1980https://doi.org/10.1152/ajpregu.1980.239.1.R42MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNeurogenic hypertension and the secrets of respirationBenedito H. Machado, Daniel B. Zoccal, and Davi J. A. Moraes1 June 2017 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 312, No. 6Tetraplegia is associated with enhanced peripheral chemoreflex sensitivity and ventilatory long-term facilitationAbdulghani Sankari, Amy T. Bascom, Anas Riehani, and M. 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