Acute blood pressure elevation during repetitive hypocapnic and
eucapnic hypoxia in rats .
Bao, Gang, Preet M. Randhawa, and Eugene C. Fletcher.
Department of Medicine, Division of Respiratory and Environmental
Medicine, Louisville Veterans Administration Medical Center and
University of Louisville School of Medicine, Louisville, KY
APStracts 3:0574A, 1996.
Using a rat model, we investigated whether episodic eucapnic hypoxia
was a more potent stimulus to acute blood pressure (BP) elevation and
bradycardia than episodic hypocapnic hypoxia, as well as what the
role of sympathetic and parasympathetic nervous system was in this
cardiovascular response. Sprague Dawley (SD) and Wistar Kyoto (WKY)
rats were exposed to repetitive 30 sec cycles of hypocapnic or
eucapnic hypoxia before and after I.V. injection of the [alpha]-1
adrenergic blocker prazosin, [alpha]-2 adrenergic blocker yohimbine,
or atropine. Eucapnic hypoxia caused a 3-fold elevation in systolic
blood pressure from baseline (83.5+/-3.5 mmHg in WKY, 70.6+/-4.6 mmHg
in SD) and greater bradycardia (-178+/-20 bpm in WKY, -178+/-21 bpm
in SD) compared to hypocapnic hypoxia (29.8+/-3.6 mmHg and -43+/-15
bpm in WKY, 19.0+/-4.1 mmHg and -45+/-12 bpm in SD). After prazosin,
the BP increase from eucapnic hypoxia was blunted, yohimbine showed
no effect, and atropine blocked the bradycardia. Direct measurement
of sympathetic nerve activity confirmed that adding CO2 to the
hypoxic gas mixture caused a 61% increase in sympathetic nerve
activity. Wistar Kyoto rats seem more vulnerable to both hypoxia
exposures than Sprague Dawley rats in terms of the elevation in BP.
We conclude that in the rat, eucapnic hypoxia is a more potent
stimulus to acute BP elevation and bradycardia than is hypocapnic
hypoxia. An increased sympathetic tone appears to be involved in the
blood pressure response to acute episodic hypoxia.
Received 12 September 1996; accepted in final form 19 November
1996.
APS Manuscript Number A877-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996