Acute blood pressure elevation during repetitive hypocapnic and eucapnic hypoxia in rats.

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. We also investigated the role of sympathetic and parasympathetic nervous system in this cardiovascular response. Sprague-Dawley (SD) and Wistar Kyoto (WKY) rats were exposed to repetitive 30-s cycles of hypocapnic or eucapnic hypoxia before and after intravenous injection of the alpha1-adrenergic blocker prazosin, alpha2-adrenergic blocker yohimbine, or atropine. Eucapnic hypoxia caused a threefold elevation in systolic BP from baseline (83.5 +/- 3.5 mmHg in WKY, 70.6 +/- 4.6 mmHg in SD) and greater bradycardia (-178 +/- 20 beats/min in WKY, -178 +/- 21 beats/min in SD) compared with hypocapnic hypoxia (29.8 +/- 3.6 mmHg and -43 +/- 15 beats/min in WKY, 19.0 +/- 4.1 mmHg and -45 +/- 12 beats/min 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. WKY rats seem more vulnerable than SD rats to both hypoxia exposures 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 BP response to acute episodic hypoxia.