scholarly journals Glucocorticoids act in the dorsal hindbrain to modulate baroreflex control of heart rate

2006 ◽  
Vol 290 (4) ◽  
pp. R1003-R1011 ◽  
Author(s):  
Andrea G. Bechtold ◽  
Deborah A. Scheuer
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Receptor Expression ◽  
Arterial Baroreflex ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Sprague Dawley Rats ◽  
Corticosteroid Receptor ◽  
Dorsal Hindbrain

Systemic corticosterone (Cort) modulates arterial baroreflex control of both heart rate and renal sympathetic nerve activity. Because baroreceptor afferents terminate in the dorsal hindbrain (DHB), an area with dense corticosteroid receptor expression, we tested the hypothesis that prolonged activation of DHB Cort receptors increases the midpoint and reduces the gain of arterial baroreflex control of heart rate in conscious rats. Small (3–4 mg) pellets of Cort (DHB Cort) or Silastic (DHB Sham) were placed on the surface of the DHB, or Cort was administered systemically by placing a Cort pellet on the surface of the dura (Dura Cort). Baroreflex control of heart rate was determined in conscious male Sprague Dawley rats on each of 4 days after initiation of treatment. Plots of arterial pressure vs. heart rate were analyzed using a four-parameter logistic function. After 3 days of treatment, the arterial pressure midpoint for baroreflex control of heart rate was increased in DHB Cort rats (123 ± 2 mmHg) relative to both DHB Sham (108 ± 3 mmHg) and Dura Cort rats (109 ± 2 mmHg, P < 0.05). On day 4, baseline arterial pressure was greater in DHB Cort (112 ± 2 mmHg) compared with DHB Sham (105 ± 2 mmHg) and Dura Cort animals (106 ± 2 mmHg, P < 0.05), and the arterial pressure midpoint was significantly greater than mean arterial pressure in the DHB Cort group only. Also on day 4, maximum baroreflex gain was reduced in DHB Cort (2.72 ± 0.12 beats·min−1·mmHg−1) relative to DHB Sham and Dura Cort rats (3.51 ± 0.28 and 3.37 ± 0.27 beats·min−1·mmHg−1, P < 0.05). We conclude that Cort acts in the DHB to increase the midpoint and reduce the gain of the heart rate baroreflex function.

Thyroid status influences baroreflex function and autonomic contributions to arterial pressure and heart rate

2001 ◽  
Vol 280 (5) ◽  
pp. H2061-H2068 ◽  
Author(s):  
C. Michael Foley ◽  
Richard M. McAllister ◽  
Eileen M. Hasser
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Logistic Function ◽  
Arterial Baroreflex ◽  
Thyroid Status ◽  
Baroreflex Control ◽  
Baroreflex Function ◽  
Resting Blood Pressure ◽  
Sympathetic Influence

The effect of thyroid status on arterial baroreflex function and autonomic contributions to resting blood pressure and heart rate (HR) were evaluated in conscious rats. Rats were rendered hyperthyroid (Hyper) or hypothyroid (Hypo) with triiodothyronine and propylthiouracil treatments, respectively. Euthyroid (Eut), Hyper, and Hypo rats were chronically instrumented to measure mean arterial pressure (MAP), HR, and lumbar sympathetic nerve activity (LSNA). Baroreflex function was evaluated with the use of a logistic function that relates LSNA or HR to MAP during infusion of phenylephrine and sodium nitroprusside. Contributions of the autonomic nervous system to resting MAP and HR were assessed by blocking autonomic outflow with trimethaphan. In Hypo rats, the arterial baroreflex curve for both LSNA and HR was shifted downward. Hypo animals exhibited blunted sympathoexcitatory and tachycardic responses to decreases in MAP. Furthermore, the data suggest that in Hypo rats, the sympathetic influence on HR was predominant and the autonomic contribution to resting MAP was greater than in Eut rats. In Hyper rats, arterial baroreflex function generally was similar to that in Eut rats. The autonomic contribution to resting MAP was not different between Hyper and Eut rats, but predominant parasympathetic influence on HR was exhibited in Hyper rats. The results demonstrate baroreflex control of LSNA and HR is attenuated in Hypo but not Hyper rats. Thyroid status alters the balance of sympathetic to parasympathetic tone in the heart, and the Hypo state increases the autonomic contributions to resting blood pressure.

Daily spontaneous running attenuated the central gain of the arterial baroreflex

1995 ◽  
Vol 268 (2) ◽  
pp. H662-H669 ◽  
Author(s):  
C. Y. Chen ◽  
S. E. DiCarlo ◽  
T. J. Scislo
Keyword(s):  
Heart Rate ◽  
Weight Ratio ◽  
Heart Weight ◽  
Arterial Baroreflex ◽  
Sprague Dawley ◽  
Baroreflex Control ◽  
Aortic Depressor Nerve ◽  
Baroreflex Function ◽  
Sprague Dawley Rats ◽  
Carotid Arterial

Exercise training attenuates arterial baroreflex function. Mechanisms responsible may include an attenuated aortic baroreceptor reactivity (afferent mechanisms) and/or an attenuated central baroreflex gain. We tested the hypothesis that the aortic baroreceptor reactivity and/or central gain is attenuated by daily spontaneous running (DSR). Eighteen anesthetized Sprague-Dawley rats (11 control and 7 DSR) were tracheotomized and instrumented with femoral venous and right carotid arterial catheters. Electrodes were placed around the left aortic depressor nerve and the lumbar sympathetic trunk. Eight to thirteen weeks of DSR were associated with a 20% increase in heart weight-to-body weight ratio (2.83 +/- 0.04 vs. 3.39 +/- 0.10 g/kg; P < 0.001) and resting bradycardia (413 +/- 6 vs. 384 +/- 10 beats/min; P = 0.01). DSR reduced the central gain of the baroreflex regulation of heart rate (0.210 +/- 0.046 vs. 0.005 +/- 0.021 beats.min-1.%-1; P = 0.004) during decreases in arterial pressure. However, the reactivity of aortic baroreceptor afferents and the central gain of the baroreflex control of lumbar sympathetic nerve activity were not different in control and DSR rats. Thus DSR reduced the central gain of the arterial baroreflex regulation of heart rate without changing the reactivity of aortic baroreceptor afferents. We conclude that afferent mechanisms are not responsible for the training-induced reduction in arterial baroreflex function.

Effect of circulating vasopressin on arterial pressure regulation in rats

1989 ◽  
Vol 257 (1) ◽  
pp. H209-H218 ◽  
Author(s):  
C. M. Pawloski ◽  
N. M. Eicker ◽  
L. M. Ball ◽  
M. L. Mangiapane ◽  
G. D. Fink
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Body Fluid ◽  
Area Postrema ◽  
Sodium Intake ◽  
Blood Levels ◽  
Fluid Composition ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Autonomic Cardiovascular Control

It has been hypothesized that moderately increased blood levels of arginine vasopressin (AVP) contribute to the development and/or maintenance of hypertension. In this study, male Sprague-Dawley rats on a fixed 1 meq daily sodium intake received 10-day intravenous infusions of 0.2 and 2.0 ng.kg-1.min-1 AVP. The higher infusion rate was above the acute vasoconstrictor threshold for AVP administration and also produced a maximal antidiuretic effect. During chronic AVP administration, however, daily mean arterial pressure, heart rate, and body fluid composition were not changed, despite a maintained antidiuresis. To test the hypothesis that circulating AVP failed to cause hypertension as a result of sensitization of the baroreflex or a direct sympathoinhibitory effect of the peptide, additional experiments were performed in rats subjected to sinoaortic denervation (SAD) or ablation of the area postrema (APX). Infusion of AVP for 10 days into SAD or APX rats caused a sustained antidiuresis but did not change arterial pressure, heart rate, or body fluid composition. In all groups of rats, the depressor response to ganglionic blockade (20 mg/kg hexamethonium) was used to estimate the autonomic component of resting arterial pressure; no change in autonomic cardiovascular control was found using this method in any of the groups during AVP infusion. Long-term elevation of plasma AVP in rats, therefore, does not cause hypertension or significantly affect autonomic regulation of arterial pressure.

Rapid resetting of baroreflexes in hypertensive dogs

1992 ◽  
Vol 262 (5) ◽  
pp. H1508-H1514
Author(s):  
M. J. Brunner ◽  
M. D. Kligman
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Carotid Sinus ◽  
Experimental Hypertension ◽  
Arterial Baroreflex ◽  
Short Term ◽  
Baroreflex Control ◽  
Pentobarbital Sodium ◽  
Reflex Gain ◽  
Pentobarbital Sodium Anesthesia

The hypothesis tested was that the rapid resetting of the arterial baroreflex control of arterial pressure in normotension could be demonstrated in experimental hypertension. After the development of experimental hypertension (using a bilateral renal wrap technique), rapid resetting of arterial pressure and heart rate (HR) was acutely assessed under pentobarbital sodium anesthesia in hypertensive and normotensive vagotomized dogs. The carotid sinus area was isolated and perfused at controlled carotid sinus pressures (CSPs). Baroreflex response [mean arterial pressure (MAP) and HR] curves were measured after three carotid sinus conditioning pressures (50, 125, and 200 mmHg) were applied. For the MAP response, the CSPo (CSP at point of maximum reflex gain) increased significantly to the same extent in both groups with increasing conditioning pressures (with 22.2 and 16.7% resetting in the normotensive group, and 20.3 and 14.2% resetting in the hypertensive group). We conclude that short-term adjustments to changes in prevailing pressure (rapid resetting) occur in the arterial pressure response in experimental hypertension to the same extent seen in normotension.

Kappa opioids modulate the arterial baroreflex control of heart rate in conscious young sheep

2007 ◽  
Vol 85 (8) ◽  
pp. 811-817 ◽  
Author(s):  
Wei Qi ◽  
Francine G. Smith
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Direct Evidence ◽  
Opiate Receptors ◽  
Random Order ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Physiological Conditions ◽  
Kappa Opioids ◽  
Before And After

The present study tested the hypothesis that κ-opioids modulate the arterial baroreflex control of heart rate in conscious young sheep. Various parameters governing the arterial baroreflex control of heart rate were assessed before and after activation of κ-opiate receptors (KOR) by i.v. administration of the specific KOR agonist U-50488H (experiment 1) or vehicle (experiment 2) to conscious, chronically instrumented lambs aged 42 ± 2 days (n = 6). The 2 experiments were administered in random order at minimum intervals of 48 h. Thirty min after U-50488H treatment, there was an increase in diastolic and mean arterial pressure and in heart rate, returning to control levels by 90 min. A significant increase in the arterial pressure at the midpoint of the baroreflex range and in the minimum heart rate as well as a significant decrease in the heart rate range over which the arterial baroreflex operates were also seen at 30 min after U-50488H, gradually returning to control levels over 120 min. Vehicle had no effect on any of the parameters governing the arterial baroreflex control of heart rate. These data provide the first direct evidence that under physiological conditions in young lambs, the arterial baroreflex control of heart rate is altered after administration of the specific KOR agonist U-50488H, revealing a previously unidentified role for this opioid receptor.

Individual differences in the heart rate response to activation of the muscle metaboreflex in humans

2010 ◽  
Vol 299 (5) ◽  
pp. H1708-H1714 ◽  
Author(s):  
Kazuhito Watanabe ◽  
Masashi Ichinose ◽  
Naoto Fujii ◽  
Mayumi Matsumoto ◽  
Takeshi Nishiyasu
Keyword(s):  
Heart Rate ◽  
Individual Differences ◽  
Arterial Pressure ◽  
Arterial Baroreflex ◽  
Frequency Range ◽  
Autonomic Tone ◽  
Isometric Handgrip ◽  
Baroreflex Control ◽  
Muscle Metaboreflex ◽  
Transfer Function Analysis

We tested the hypotheses that the heart rate (HR) response to muscle metaboreflex activation induced by postexercise muscle ischemia (PEMI) varies considerably among subjects and that individual differences in the HR response are associated with differences in cardiac autonomic tone and/or arterial baroreflex function during PEMI. Fifty-one healthy subjects (36 men and 15 women) performed a 1-min isometric handgrip exercise at 50% maximal voluntary contraction, which was followed by a 3.5-min period of imposed PEMI. We estimated cardiac autonomic tone using spectral analysis of beat-to-beat variation in the R-R interval (RRI). In addition, the sensitivity of the arterial baroreflex control of HR (BRS) was evaluated using transfer function analysis of systolic arterial pressure (SAP) and RRI. Although the mean RRI during the PEMI and subsequent recovery period did not differ from the resting value, the variance among the individual differences in RRI between the rest and PEMI periods was significantly greater than between the rest and recovery periods. The changes in RRI elicited by PEMI correlated significantly with changes in the spectral power of the RRI variability in the high-frequency range and the BRS. By contrast, no significant correlation was observed between changes in RRI and changes in mean arterial pressure or the power of the RRI variability in the low-frequency range. This suggests that, in humans, the HR response to PEMI-induced activation of muscle metaboreflex varies considerably from individual to individual and that these differences reflect changes in cardiac parasympathetic tone and spontaneous BRS during PEMI.

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

1984 ◽  
Vol 246 (1) ◽  
pp. H80-H89 ◽  
Author(s):  
G. B. Guo ◽  
F. M. Abboud
Keyword(s):  
Heart Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Reflex Inhibition ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Excitatory Effect ◽  
Baroreflex Control ◽  
Reflex Bradycardia ◽  
Background Infusion

We determined whether angiotensin II (ANG II) modulates the arterial baroreflex control of lumbar sympathetic nerve activity (LSNA) in chloralose-anesthetized rabbits. Intravenous infusion (iv) of ANG II caused significantly less reflex bradycardia and less inhibition of LSNA than iv phenylephrine (PE) for equivalent increments in arterial pressure. During a background iv infusion of ANG II, which caused a small sustained increase in arterial pressure, the reflex inhibition of heart rate (HR) and LSNA in response to further increases in pressure with graded doses of PE was attenuated, but the reflex increase in HR and LSNA in response to hypotension with graded doses of nitroprusside was unchanged. This modulation of the baroreflex by ANG II is specific since a similar background infusion of PE did not alter baroreflex responses to further increases or to decreases in arterial pressure. The frequency of aortic baroreceptors was comparable for equivalent increases in pressure caused by iv ANG II or PE. When ANG II was confined to the isolated carotid sinuses, the reflex inhibition of HR and LSNA during distension of carotid sinuses was unchanged. An excitatory effect of ANG II on the efferent limb of the baroreflex that would oppose the reflex bradycardia or inhibition of LSNA is unlikely because when the pressor effect of ANG II was prevented by nitroprusside, there were no changes in HR and LSNA. We conclude that through an effect on the central nervous system iv ANG II has a selective effect on the arterial baroreflex; it impairs reflex decreases in HR and LSNA during hypertension but not reflex increases in HR and LSNA during hypotension.

Exercise training enhances baroreflex control of heart rate by a vagal mechanism in rabbits with heart failure

2002 ◽  
Vol 92 (6) ◽  
pp. 2403-2408 ◽  
Author(s):  
Jun-Li Liu ◽  
Jay Kulakofsky ◽  
Irving H. Zucker
Keyword(s):  
Heart Failure ◽  
Heart Rate ◽  
Exercise Training ◽  
Arterial Pressure ◽  
Normal Subjects ◽  
Work Capacity ◽  
Logistic Function ◽  
Baroreflex Control ◽  
Before And After

Moderate exercise training (Ex) enhances work capacity and quality of life in patients with chronic heart failure (CHF). We investigated the autonomic components of resting heart rate (HR) and the baroreflex control of HR in conscious, instrumented rabbits with pacing-induced CHF after Ex. Sham and CHF rabbits were exercise trained for 4 wk at 15–18 m/min, 6 days/wk. Arterial pressure and HR were recorded before and after metoprolol (1 mg/kg iv) or after atropine (0.2 mg/kg iv). Mean arterial pressure was altered by infusions of sodium nitroprusside and phenylephrine. The data were fit to a sigmoid (logistic) function. Baseline HRs were 266.5 ± 8.4 and 232.1 ± 1.6 beats/min in CHF and CHF Ex rabbits, respectively ( P < 0.05). In the unblocked state, CHF rabbits had a significantly depressed peak baroreflex slope (1.7 ± 0.3 vs. 5.6 ± 0.7 beats · min−1 · mmHg−1; P < 0.001) and HR range (128.6 ± 34.5 vs. 253.2 ± 20.3 beats/min; P < 0.05) compared with normal subjects. Ex increased baroreflex slope to 4.9 ± 0.3 from 1.7 ± 0.3 beats · min−1 · mmHg−1 in unblocked rabbits ( P < 0.001 compared with CHF non-Ex). Ex did not alter baroreflex function in sham animals. After metoprolol, baroreflex slope was significantly increased in CHF Ex rabbits (1.5 ± 0.2 vs. 3.0 ± 0.2 beats · min−1 · mmHg−1; P < 0.05). After atropine, there was no significant change in baroreflex slope or HR range between CHF Ex and CHF rabbits. These data support the view that enhancement of baroreflex control of HR after Ex is due to an augmentation of vagal tone.

Chronic Lability of Arterial Pressure in the Rat Does Not Evolve into Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 405s-407s ◽  
Author(s):  
W. T. Talman ◽  
D. R. Alonso ◽  
D. J. Reis
Keyword(s):  
Heart Rate ◽  
Standard Deviation ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Histopathological Changes ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Electrolytic Lesions ◽  
The Mean ◽  
Catecholamine Neurons

1. In rats, electrolytic lesions of the A2 group of catecholamine neurons result in lability of arterial pressure without hypertension. 2. To establish whether labile arterial pressure, when chronic, will lead to fixed hypertension, we placed lesions in the A2 area of adult male Sprague-Dawley rats and measured mean arterial pressure, heart rate and their variability (expressed as the standard deviation) 11 months later. Controls were age-matched, unoperated or sham-operated rats. 3. In rats with A2 lesions: (a) the mean arterial pressure was lower (103 ± 7.5 mmHg; n = 6; P&lt;0.05) than in sham-operated (123 ± 4.7 mmHg; n = 4) or unoperated (120 ± 3.1 mmHg; n = 9) controls; (b) the standard deviation of mean arterial pressure was higher (16 ± 1.8 mmHg; P&lt;0.001) than in sham-operated (5 ± 0.7 mmHg) or unoperated controls (7 ± 0.6 mmHg); (c) the mean and standard deviation of heart rate did not differ between groups. No histopathological changes were detected in the A2 group. 4. Chronic lability of arterial pressure does not evolve into sustained hypertension nor does it induce systemic lesions.

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