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This Article Full Text Full Text (PDF) All Versions of this Article: 92/1/45    most recent expphysiol.2006.033753v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Smith, M. L. Articles by Pacchia, C. F. Search for Related Content PubMed PubMed Citation Articles by Smith, M. L. Articles by Pacchia, C. F. Related Collections Themed Issue papers

¹ Department of Integrative Physiology, University of North Texas Health Science Center, Fort Worth, TX, USA

The link between sleep apnoea and systemic hypertension in humans is well documented. However, a direct causal association between the two diseases independent of comorbidities has been difficult to establish. Comorbidities 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 a result of chronically elevated sympathetic activity, and therefore 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, 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 are explored in this review. Thus, this review focuses on the current evidence linking chemoreflex function to obstructive sleep apnoea and systemic hypertension in humans and provides an analysis of these data and their implications.

(Received 26 September 2006; accepted after revision 9 November 2006; first published online 10 November 2006)
Corresponding author M. L. Smith: Department of Integrative Physiology, University of North Texas Health Science Center, 3500 Camp Bowie Boulevard, Fort Worth, TX 76107, USA. Email: msmith{at}hsc.unt.edu