Title

Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice

Authors

Authors

M. Lin; R. G. Liu; D. Gozal; W. B. Wead; M. W. Chapleau; R. Wurster;Z. J. Cheng

Comments

Authors: contact us about adding a copy of your work at STARS@ucf.edu

Abbreviated Journal Title

Am. J. Physiol.-Heart Circul. Physiol.

Keywords

nucleus ambiguus; obstructive sleep apnea; cardiac ganglia; OBSTRUCTIVE SLEEP-APNEA; SYMPATHETIC-NERVE ACTIVITY; NUCLEUS AMBIGUUS; CARDIOVASCULAR FUNCTION; SYSTEMIC HYPERTENSION; BARORECEPTOR REFLEX; ARTERIAL-PRESSURE; OXIDATIVE STRESS; CARDIAC GANGLIA; FOS EXPRESSION; Cardiac & Cardiovascular Systems; Physiology; Peripheral Vascular; Disease

Abstract

Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice. Am J Physiol Heart Circ Physiol 293: H997 - H1006, 2007. First published March 23, 2007; doi:10.1152/ajpheart.01124.2006. - Chronic intermittent hypoxia ( CIH) leads to increased sympathetic nerve activity and arterial hypertension. In this study, we tested the hypothesis that CIH impairs baroreflex ( BR) control of heart rate (HR) in mice, and that decreased cardiac chronotropic responsiveness to vagal efferent activity contributes to such impairment. C57BL/6J mice were exposed to either room air (RA) or CIH (6-min alternations of 21% O-2 and 5.7% O-2, 12 h/day) for 90 days. After the treatment period, mice were anesthetized ( Avertin) and arterial blood pressure (ABP) was measured from the femoral artery. Mean ABP ( MABP) was significantly increased in mice exposed to CIH (98.7 +/- 2.5 vs. RA: 78.9 +/- 1.4 mmHg, P < 0.001). CIH increased HR significantly (584.7 +/- 8.9 beats/ min; RA: 518.2 +/- 17.9 beats/min, P < 0.05). Sustained infusion of phenylephrine (PE) at different doses (0.1 - 0.4 mu g/min) significantly increased MABP in both CIH and RA mice, but the ABP-mediated decreases in HR were significantly attenuated in mice exposed to CIH ( P < 0.001). In contrast, decreases in HR in response to electrical stimulation of the left vagus nerve ( 30 mu A, 2-ms pulses) were significantly enhanced in mice exposed to CIH compared with RA mice at low frequencies. We conclude that CIH elicits a sustained impairment of baroreflex control of HR in mice. The blunted BR-mediated bradycardia occurs despite enhanced cardiac chronotropic responsiveness to vagal efferent stimulation. This suggests that an afferent and/or a central defect is responsible for the baroreflex impairment following CIH.

Journal Title

American Journal of Physiology-Heart and Circulatory Physiology

Volume

293

Issue/Number

2

Publication Date

1-1-2007

Document Type

Article

Language

English

First Page

H997

Last Page

H1006

WOS Identifier

WOS:000248488000013

ISSN

0363-6135

Share

COinS