Received September 26, 2006
Revised October 10, 2006
Accepted after revision November 9, 2006

¹ University of North Texas

^* To whom correspondence should be addressed. E-mail: msmith{at}hsc.unt.edu.

	Abstract

The link between sleep apnoea and systemic hypertension in humans is well-documented. However, a direct causal association between the two diseases independent of co-morbidities has been difficult to establish. Co-morbidities clearly play an important role in this strong relationship, however, new findings also suggest that sleep apnoea is an independent risk factor for hypertension. This relationship appears to be at least in part due to chronically elevated sympathetic activity, and thus, manifests as a neurally-mediated hypertension. Although the mechanism(s) for this causal relationship of sleep apnoea to hypertension remains ill-defined, a growing body of literature suggests that autonomic dysfunction as mediated by abnormal chemoreflex control of sympathetic activity is a potential mechanism. Abnormal chemoreflex responses to both acute and chronic apnoea or hypoxia have been demonstrated. Hypothesized mechanisms by which chemoreflex dysfunction may contribute to chronically elevated sympathetic tone and ultimately hypertension is explored in this review. Thus, this review focuses on the current evidence linking chemoreflex function to OSA and systemic hypertension in humans and provides an analysis of these data and their implications.

Key Words: Chemoreceptor, Hypertension, Hypoxia

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