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First published online on November 23, 2006.
Experimental Physiology (2006)
DOI: 10.1113/expphysiol.2006.035204
© The Physiological Society 2006
A more recent version of this article appeared on January 1, 2007
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Received September 5, 2006
Revised October 12, 2006
Accepted after revision November 15, 2006

Cardiovascular Control [210]

Intermittent hypoxia and vascular function: implications for obstructive sleep apnea

Glen E Foster 1, Marc J Poulin 1*, Patrick J Hanly 1

1 University of Calgary

* To whom correspondence should be addressed. E-mail: poulin{at}ucalgary.ca.


  Abstract
Obstructive sleep apnea (OSA) has been implicated as a risk factor for the development of hypertension, stroke, and myocardial infarction. The main cause of cardiovascular and cerebrovascular disease in OSA is thought to be exposure to intermittent hypoxia, which can lead to oxidative stress, inflammation, atherosclerosis, endothelial dysfunction, and hypertension. These proposed mechanisms have been drawn from basic research in animal and human models of intermittent hypoxia in addition to clinical investigation of patients with OSA. This review outlines the association between OSA and vascular disease, describes basic mechanisms that may be responsible for this association, and compares the results from studies of OSA subjects with those in experimental models of intermittent hypoxia.

Key Words: Cardiovascular, Hypertension, Hypoxia




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