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Chronic intermittent hypoxia impairs baroreflex control of heart rate but enhances heart rate responses to vagal efferent stimulation in anesthetized mice
Journal article   Open access   Peer reviewed

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

Min Lin, Rugao Liu, David Gozal, William B Wead, Mark W Chapleau, Robert Wurster and Zixi Jack Cheng
American journal of physiology. Heart and circulatory physiology, Vol.293(2), pp.H997-1006
08/2007
DOI: 10.1152/ajpheart.01124.2006
PMID: 17384123
url
https://stars.library.ucf.edu/facultybib2000/7360View
Open Access

Abstract

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 microg/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 microA, 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.
 Anesthesia, General Electric Stimulation Afferent Pathways - physiopathology Vagus Nerve - drug effects Nitroprusside - pharmacology Tachycardia - etiology Hypertension - etiology Dose-Response Relationship, Drug Heart Rate - drug effects Ethanol - analogs & derivatives Phenylephrine - pharmacology Blood Pressure - drug effects Disease Models, Animal Heart - innervation Vasodilator Agents - pharmacology Mice, Inbred C57BL Hypoxia - complications Anesthetics Tachycardia - physiopathology Hypertension - physiopathology Efferent Pathways - physiopathology Vagus Nerve - physiopathology Baroreflex - drug effects Animals Heart - drug effects Adrenergic alpha-Agonists - pharmacology Hypoxia - physiopathology Mice Chronic Disease

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