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Treatment of obstructive sleep apnoea leads to improved microvascular endothelial function in the systemic circulation
  1. J L Lattimore1,2,
  2. I Wilcox1,2,
  3. M Skilton1,2,
  4. M Langenfeld1,2,
  5. D S Celermajer1,2
  1. 1Department of Cardiology, Royal Prince Alfred Hospital Sydney, NSW, Australia
  2. 2Department of Medicine, University of Sydney, NSW, Australia
  1. Correspondence to:
    Dr J L Lattimore
    Department of Cardiology, Royal Prince Alfred Hospital, Missenden Road, Camperdown, NSW 2050, Sydney, Australia; jodee.lattimore{at}


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. Microvascular arterial endothelial and smooth muscle function was assessed in subjects with OSA before and after treatment with continuous positive airways pressure (CPAP).

Methods: Ten subjects of mean (SE) age 49 (8) years with at least moderately severe OSA had detailed forearm vascular reactivity studies before and after 3 months of CPAP treatment. 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).

Results: Before CPAP, ACh and SNP infusions increased forearm blood flow in a dose dependent manner (p<0.01). After CPAP, endothelium dependent dilation to ACh was significantly increased (434 (23)% of baseline after CPAP v 278 (20)% before CPAP, p<0.001), whereas SNP induced dilation was unchanged. Resting NO production was higher after CPAP, evidenced by a significantly greater reduction in basal flow by l-NMMA (p = 0.05). l-Arginine reversed the effect of l-NMMA in all cases.

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

  • ACh, acetylcholine
  • AHI, apnoea hypopnoea index
  • BMI, body mass index
  • CPAP, continuous positive airway pressure
  • l-NMMA, NG-monomethyl-l-arginine
  • NO, nitric oxide
  • OSA, obstructive sleep apnoea
  • SNP, sodium nitroprusside
  • hypertension
  • atherosclerosis
  • nitric oxide
  • obstructive sleep apnoea
  • continuous positive airway pressure

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