Treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the systemic circulation

Jo-Dee L Lattimore ^1*, Ian Wilcox ¹, Michael Skilton ¹, Matthias Langenfeld ¹ and David S Celermajer ¹

¹ Royal Prince Alfred Hospital, Australia

^* To whom correspondence should be addressed. E-mail: jodee.lattimore{at}email.cs.nsw.gov.au.

Accepted 17 January 2006

Abstract

Background: Obstructive sleep apnoea (OSA) is a common and potentially reversible cause of systemic hypertension. The mechanisms whereby OSA leads to hypertension and the effects of treatment on arterial function, however, are not well established. We therefore assessed microvascular arterial endothelial and smooth muscle function in subjects with OSA, before and after treatment with continuous positive airways pressure (CPAP).

Methods and results: Ten subjects aged 49 ±8 years (±SD) with at least moderately severe OSA had detailed forearm vascular reactivity studies, before and after 3 months of CPAP. The systemic circulation was assessed by measuring brachial artery pressure, flow and resistance responses to intra-arterial infusions of acetylcholine (ACh - an endothelium dependent vasodilator), sodium nitroprusside (SNP - an endothelium independent vasodilator), L-NMMA (a nitric oxide - NO-antagonist) and L-arginine (the substrate for NO). Before CPAP, ACh and SNP infusions increased forearm blood flow in a dose- dependent manner (p<0.001). After CPAP, endothelium-dependent dilation to ACh was significantly increased (434±23% of baseline post-CPAP vs 278±20% pre-CPAP, p<0.001), whereas SNP-induced dilation was unchanged. Resting NO production was higher after CPAP, evidenced by a greater reduction in basal flow by L-NMMA (p=0.05). L-arginine reversed the L-NMMA effect in all cases.

Conclusion: In patients with OSA, CPAP therapy improves baseline endothelial NO release and stimulates endothelium-dependent vasorelaxation in the systemic circulation. This is a potential mechanism for improvement in systemic and vascular function in patients with OSA treated with CPAP.

Keywords: atherosclerosis, hypertension, nitric oxide

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