Age-related changes in baroreflex control of heart rate and sympathetic nerve activity in healthy humans

Recent data suggest that nitric oxide (NO) plays a role in the modulation of sympathetic nerve activity and baroreflex sensitivity. Most of these studies have been carried out in anesthetized preparations, and little if any comparison has been made on the relative role of NO on the baroreflex control of heart rate and sympathetic nerve activity. In the present studies, the effect of the NO synthase inhibitor NG-nitro-L-arginine (L-NNA) on the baroreflex control of heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in conscious, instrumented rabbits. Intravenous bolus injections of 13 mg/kg of L-NNA decreased baseline HR (from 205.0 +/- 6.0 to 145.5 +/- 8.2 beats/min; P < 0.05) without significant changes in mean arterial pressure (MAP) and RSNA. L-NNA significantly reduced the lower plateau of the HR-MAP curves and increased the sensitivities of baroreflex control of HR and RSNA. L-Arginine (600 mg/kg i.v.) but not D-arginine reversed the above effects. The effects of L-NNA on baseline HR were not completely blocked by metoprolol (2 mg/kg) or by atropine (0.2 mg/kg). After pretreatment with metoprolol, baroreflex sensitivity was reduced and L-NNA increased baroreflex sensitivity back to the control level. After pretreatment with atropine, L-NNA still reduced the lower plateau but did not significantly affect baroreflex sensitivity. L-NNA increased the HR responses but not the RSNA response to electrical stimulation of the aortic nerve in chloralose-anesthetized, sinoaortic-denervated (SAD) rabbits. L-NNA had no effect on the HR response to right vagal stimulation. In both conscious intact and SAD rabbits, L-NNA did not increase baseline RSNA. These results suggest that endogenous NO decreases baroreflex control of HR and RSNA. Both sympathetic and parasympathetic components play a role in the effects of NO on the baroreflex control of HR. The effects of NO in the central nervous system play a more important role in the baroreflex control of HR than of RSNA.

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

Circulation ◽

10.1161/01.cir.80.2.285 ◽

1989 ◽

Vol 80 (2) ◽

pp. 285-298 ◽

Cited By ~ 27

Author(s):

D W Ferguson ◽

D W Hayes

Keyword(s):

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Direct Evidence ◽

Nerve Activity ◽

Baroreflex Control ◽

Healthy Humans ◽

Cardiopulmonary Baroreflex

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The Effect of Residential Exercise Training on Baroreflex Control of Heart Rate and Sympathetic Nerve Activity in Patients With Acute Myocardial Infarction

CHEST Journal ◽

10.1016/s0012-3692(15)34454-8 ◽

2005 ◽

Vol 127 (4) ◽

pp. 1108-1115 ◽

Cited By ~ 2

Author(s):

Jun Mimura ◽

Fumio Yuasa ◽

Reisuke Yuyama ◽

Akihiro Kawamura ◽

Masayoshi Iwasaki ◽

...

Keyword(s):

Myocardial Infarction ◽

Acute Myocardial Infarction ◽

Heart Rate ◽

Exercise Training ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Nerve Activity ◽

Baroreflex Control

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Influence of increased central venous pressure on baroreflex control of sympathetic activity in humans

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.00265.2004 ◽

2004 ◽

Vol 287 (4) ◽

pp. H1658-H1662 ◽

Cited By ~ 62

Author(s):

N. Charkoudian ◽

E. A. Martin ◽

F. A. Dinenno ◽

J. H. Eisenach ◽

N. M. Dietz ◽

...

Keyword(s):

Heart Rate ◽

Arterial Pressure ◽

Sympathetic Activity ◽

Sympathetic Nerve Activity ◽

Venous Pressure ◽

Central Venous ◽

Nerve Activity ◽

Baroreflex Control ◽

Healthy Humans ◽

Rapid Changes

Volume expansion often ameliorates symptoms of orthostatic intolerance; however, the influence of this increased volume on integrated baroreflex control of vascular sympathetic activity is unknown. We tested whether acute increases in central venous pressure (CVP) diminished subsequent responsiveness of muscle sympathetic nerve activity (MSNA) to rapid changes in arterial pressure. We studied healthy humans under three separate conditions: control, acute 10° head-down tilt (HDT), and saline infusion (SAL). In each condition, heart rate, arterial pressure, CVP, and peroneal MSNA were measured during 5 min of rest and then during rapid changes in arterial pressure induced by sequential boluses of nitroprusside and phenylephrine (modified Oxford technique). Sensitivities of integrated baroreflex control of MSNA and heart rate were assessed as the slopes of the linear portions of the MSNA-diastolic blood pressure and R-R interval-systolic pressure relations, respectively. CVP increased ∼2 mmHg in both SAL and HDT conditions. Resting heart rate and mean arterial pressure were not different among trials. Sensitivity of baroreflex control of MSNA was decreased in both SAL and HDT condition, respectively: −3.1 ± 0.6 and −3.3 ± 1.0 versus −5.0 ± 0.6 units·beat−1·mmHg−1 ( P < 0.05 for SAL and HDT vs. control). Sensitivity of baroreflex control of the heart was not different among conditions. Our results indicate that small increases in CVP decrease the sensitivity of integrated baroreflex control of sympathetic nerve activity in healthy humans.

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