Hypoxia 2009 Speakers |
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Barbara Morgan |
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| Talk Title: Vascular Consequences Of Intermittent Hypoxia | |
| Session: Vascular, Metabolic, and Cognitive Effects of Intermittent Hypoxia | |
| Abstract: Obstructive sleep apnea (OSA) is associated with hypertension and other forms of cardiovascular morbidity. OSA-related hypertension is characterized by sympathetic nervous system overactivity and impaired vascular endothelial function. Although episodes of OSA impose multiple insults, intermittent hypoxia, rather than hypercapnia, arousals, or intrathoracic pressure oscillations, is the most important pro-hypertensive factor. In experimental animals, exposure to intermittent hypoxia during sleep causes elevations in arterial pressure that persist throughout the day. This hypertensive effect requires an intact sympathetic nervous system and an intact carotid chemoreceptor reflex. The renin-angiotensin system contributes importantly to hypertension in this model, because renal nerve denervation, angiotensin II receptor blockade, and suppression of the renin-angiotensin system by high salt diet all prevent the rise in blood pressure. Although the precise pathogenetic mechanisms are unknown, existing evidence suggests that exposure to intermittent hypoxia alters vascular structure and function. Increased carotid intima-media thickness and increased arterial stiffness have been observed in individuals with OSA. Putative mechanisms for vascular remodeling include hypoxic stimulation of mitogenic factors; altered balance between extra-cellular matrix metalloproteinases and their inhibitors induced by chronic inflammation; stimulation of the local vascular renin-angiotensin system via cyclical stretch of vascular smooth muscle cells; and the trophic effects of chronic sympathetic activation. | |
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Hypoxia and the Circulation
10-15 March 2009
Chateau Lake Louise
Alberta, Canada