Baroreflex control of sinus node during dynamic exercise in humans: effects of central command and muscle reflexes

1997 ◽  
Vol 272 (3) ◽  
pp. H1157-H1164 ◽  
Author(s):  
F. Iellamo ◽  
J. M. Legramante ◽  
G. Raimondi ◽  
G. Peruzzi
Keyword(s):  
Arterial Pressure ◽  
Sinus Node ◽  
Knee Extension ◽  
Dynamic Exercise ◽  
Free Flow ◽  
Cardiac Response ◽  
Central Command ◽  
Arterial Baroreflex ◽  
Flow Conditions ◽  
Baroreflex Control

This study evaluated the influence of central command and muscle afferent stimulation (mechanical and chemical) on the integrated arterial baroreflex control of the sinus node during dynamic exercise. Twenty-two healthy men performed voluntary knee extension and electrically induced dynamic knee extension under free-flow and arrested-flow (n = 18) conditions. Systolic arterial pressure (SAP) and pulse interval (PI) were measured continuously and noninvasively. The arterial baroreflex was evaluated by analyzing the slopes of sequences of three or more consecutive beats characterized by the SAP and PI of the following beat; both increased or decreased in a linear fashion. Compared with rest, both voluntary exercise and electrically induced exercise under arrested-flow conditions resulted in a maintained baroreflex sensitivity (BRS; 11.7 +/- 1.2 vs. 9.6 +/- 0.7 and 11.3 +/- 1.4 vs. 9.8 +/- 1.5 ms/mmHg, respectively; not significant), with an apparent rightward shift in the regression line relating SAP to PI. Electrically induced exercise under free-flow conditions resulted in a significant decrease in BRS (12.1 +/- 1.4 vs. 8.8 +/- 0.8 ms/mmHg; P < 0.05). These data suggest that the central command and muscle chemoreflex act to preserve the BRS, possibly "resetting" the baroreceptor-cardiac response relationship, whereas stimulation of mechanosensitive receptors appears capable of modifying the integrated baroreflex control of sinus node function in humans. The first two mechanisms seem, however, to overwhelm the latter to maintain BRS, thus permitting a concomitant increase in arterial pressure and heart rate.

Carotid baroreflex function during and following voluntary apnea in humans

2003 ◽  
Vol 285 (6) ◽  
pp. H2411-H2419 ◽  
Author(s):  
N. Muenter Swift ◽  
M. J. Cutler ◽  
P. J. Fadel ◽  
W. L. Wasmund ◽  
S. Ogoh ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Cardiac Response ◽  
Inhibitory Input ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Carotid Baroreflex ◽  
Neck Pressure ◽  
Voluntary Apnea

Muscle sympathetic nerve activity (MSNA) and arterial pressure increase concomitantly during apnea, suggesting a possible overriding of arterial baroreflex inhibitory input to sympathoregulatory centers by apnea-induced excitatory mechanisms. Apnea termination is accompanied by strong sympathoinhibition while arterial pressure remains elevated. Therefore, we hypothesized that the sensitivity of carotid baroreflex control of MSNA would decrease during apnea and return upon apnea termination. MSNA and heart rate responses to –60-Torr neck suction (NS) were evaluated during baseline and throughout apnea. Responses to +30-Torr neck pressure (NP) were evaluated during baseline and throughout 1 min postapnea. Apnea did not affect the sympathoinhibitory or bradycardic response to NS ( P > 0.05); however, whereas the cardiac response to NP was maintained postapnea, the sympathoexcitatory response was reduced for 50 s ( P < 0.05). These data demonstrate that the sensitivity of carotid baroreflex control of MSNA is not attenuated during apnea. We propose a transient rightward and upward resetting of the carotid baroreflex-MSNA function curve during apnea and that return of the function curve to, or more likely beyond, baseline (i.e., a downward and leftward shift) upon apnea termination may importantly contribute to the reduced sympathoexcitatory response to NP.

Cardiovascular and Valsalva responses during parabolic flight

1998 ◽  
Vol 85 (5) ◽  
pp. 1957-1965 ◽  
Author(s):  
Todd T. Schlegel ◽  
Edgar W. Benavides ◽  
Donald C. Barker ◽  
Troy E. Brown ◽  
Deborah L. Harm ◽  
...  
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Human Subjects ◽  
Parabolic Flight ◽  
Cardiovascular Responses ◽  
Systematic Evaluation ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Flight Measurements

We investigated the integrated cardiovascular responses of 15 human subjects to the acute gravitational changes (micro- and hypergravity portions) of parabolic flight. Measurements were made with subjects quietly seated and while subjects performed controlled Valsalva maneuvers. During quiet, seated, parabolic flight, mean arterial pressure increased during the transition into microgravity but decreased as microgravity was sustained. The decrease in mean arterial pressure was accompanied by immediate reflexive increases in heart rate but by absent (or later-than-expected) reflexive increases in total vascular resistance. Mean arterial pressure responses in Valsalva phases IIl, III, and IV were accentuated in hypergravity relative to microgravity ( P < 0.01, P < 0.01, and P < 0.05, respectively), but accentuations differed qualitatively and quantitatively from those induced by a supine-to-seated postural change in 1 G. This study is the first systematic evaluation of temporal and Valsalva-related changes in cardiovascular parameters during parabolic flight. Results suggest that arterial baroreflex control of vascular resistance may be modified by alterations of cardiopulmonary, vestibular, and/or other receptor activity.

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.

Angiotensin II modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism in rabbits

1995 ◽  
Vol 269 (5) ◽  
pp. R1009-R1016 ◽  
Author(s):  
Y. Nishida ◽  
K. L. Ryan ◽  
V. S. Bishop
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Ang Ii ◽  
Arterial Baroreflex ◽  
Baroreflex Control ◽  
Renal Sympathetic Nerve Activity ◽  
Baroreflex Function ◽  
Before And After ◽  
Dose Dependent ◽  
Renal Sympathetic

To test the hypothesis that angiotensin II (ANG II) modulates arterial baroreflex function via a central alpha 1-adrenoceptor mechanism, we examined the effects of intravertebral infusion of ANG II on baroreflex function curves before and after intravertebral administration of the alpha 1-adrenoreceptor antagonist prazosin. Rabbits were chronically instrumented with subclavian and vertebral arterial catheters, venous catheters, and aortic and vena caval occludes. Baroreflex curves were obtained by relating heart rate (HR) to mean arterial pressure during increases and decreases in arterial pressure. Intravertebral infusions of ANG II (5, 10, and 20 ng.kg-1.min-1) produced a dose-dependent shift of the midrange of the curve toward higher pressures (64 +/- 1 to 68 +/- 1, 76 +/- 1, and 85 +/- 2 mmHg, respectively). Pretreatment with prazosin (10 micrograms/kg) via the vertebral artery markedly reduced the shift in the baroreflex curve induced by the highest dose of ANG II (64 +/- 2 to 70 +/- 2 mmHg). These data suggest that ANG II resets the operating point of the HR baroreflex curve to a higher blood pressure and that this effect is mediated via a central alpha 1 mechanism. When the effects of vertebral ANG II on the baroreflex control of renal sympathetic nerve activity (RSNA) were examined, intravertebral administration of ANG II, while reducing the gain and the maximum RSNA, did not reset the RSNA baroreflex curve. These data suggest that ANG II acutely resets the HR baroreflex but not the RSNA baroreflex and that the resetting involves an alpha 1-adrenergic mechanism.

scholarly journals Neural Regulation of Cardiovascular Response to Exercise: Role of Central Command and Peripheral Afferents

2014 ◽  
Vol 2014 ◽  
pp. 1-20 ◽  
Author(s):  
Antonio C. L. Nobrega ◽  
Donal O'Leary ◽  
Bruno Moreira Silva ◽  
Elisabetta Marongiu ◽  
Massimo F. Piepoli ◽  
...  
Keyword(s):  
Cardiovascular Response ◽  
Dynamic Exercise ◽  
Central Command ◽  
Arterial Baroreflex ◽  
Metabolic Demand ◽  
Excessive Pressure ◽  
Arterial Blood ◽  
Peripheral Afferents ◽  
Response To Exercise

During dynamic exercise, mechanisms controlling the cardiovascular apparatus operate to provide adequate oxygen to fulfill metabolic demand of exercising muscles and to guarantee metabolic end-products washout. Moreover, arterial blood pressure is regulated to maintain adequate perfusion of the vital organs without excessive pressure variations. The autonomic nervous system adjustments are characterized by a parasympathetic withdrawal and a sympathetic activation. In this review, we briefly summarize neural reflexes operating during dynamic exercise. The main focus of the present review will be on the central command, the arterial baroreflex and chemoreflex, and the exercise pressure reflex. The regulation and integration of these reflexes operating during dynamic exercise and their possible role in the pathophysiology of some cardiovascular diseases are also discussed.

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.

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.

Dynamic exercise shifts the operating point and reduces the gain of the arterial baroreflex in rats

1998 ◽  
Vol 275 (6) ◽  
pp. R2043-R2048 ◽  
Author(s):  
Heather R. Burger ◽  
Margaret P. Chandler ◽  
David W. Rodenbaugh ◽  
Stephen E. DiCarlo
Keyword(s):  
Pressure Range ◽  
Dynamic Exercise ◽  
Treadmill Running ◽  
Operating Point ◽  
Arterial Baroreflex ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
The Relationship ◽  
Carotid Arterial

We tested the hypothesis that dynamic exercise resets the operating point and attenuates the gain of the arterial baroreflex regulation of heart rate (HR) in rats. Seven adult female spontaneously hypertensive rats (SHR) were chronically instrumented with left carotid arterial catheters. After the rats recovered, arterial baroreflex function was examined by recording reflex changes in HR in response to spontaneous changes in arterial pressure (AP) during a preexercise condition and during steady-state treadmill running at 6 and 18 m/min. Dynamic exercise at 6 and 18 m/min, respectively, reduced the spontaneous range (by 55 and 70%) and spontaneous gain (by 64 and 82%) of the arterial baroreflex control of HR. Dynamic exercise at 6 and 18 m/min, respectively, also increased the pressure at the midpoint of the spontaneous pressure range (by 7 and 12%), the spontaneous minimum HR response (by 35 and 59%), the HR at the midpoint of the spontaneous HR range (by 31 and 52%), and the spontaneous maximum HR response (by 27 and 46%). Sinoaortic denervation eliminated the relationship between AP and HR by reducing the spontaneous gain 95%. These results demonstrate that dynamic exercise shifted the operating point of the arterial baroreflex to a higher pressure and reduced the spontaneous gain in female SHR.

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.

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