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Angiotensin Receptor Expression and Vascular Endothelial Dysfunction in Obstructive Sleep Apnea
Rami N Khayat1,2, Saradhadevi Varadharaj3, Kyle Porter4
1Department of Internal Medicine, The Sleep Heart Program, The Ohio State University, USA.
American Journal of Hypertension
|October 17, 2017
Summary
Obstructive sleep apnea (OSA) causes vascular endothelial dysfunction (VED) linked to renin-angiotensin system (RAS) activation. Continuous positive airway pressure (CPAP) therapy reverses this, suggesting RAS plays a role in early cardiovascular disease risk.
Area of Science:
- Cardiovascular Research
- Sleep Medicine
- Endocrinology
Background:
- Obstructive sleep apnea (OSA) is linked to vascular endothelial dysfunction (VED) in healthy individuals.
- The role of the renin-angiotensin system (RAS) in OSA-induced VED is not fully understood.
Purpose of the Study:
- To investigate the role of RAS in OSA-induced VED.
- To assess the impact of continuous positive airway pressure (CPAP) therapy on RAS components in OSA patients with low cardiovascular disease (CVD) risk.
Main Methods:
- 11 recently diagnosed OSA patients with low CVD risk were studied at baseline and after 12 weeks of CPAP.
- Gluteal subcutaneous tissue biopsies were analyzed for angiotensin receptor type-1 (AT-1) and type-2 (AT-2) expression.
- Ex-vivo effects of AT-1 receptor blockade (ARB) on endothelial superoxide production were measured.
Main Results:
- Microcirculatory endothelial AT-1 expression significantly decreased after CPAP therapy (P = 0.02).
- AT-2 expression showed no significant change post-CPAP (P = 0.08).
- ARB significantly reduced superoxide production in pre-CPAP tissue but not post-CPAP tissue.
Conclusions:
- VED in OSA patients with low CVD risk is associated with increased AT-1 expression, which is reversible with CPAP.
- Endothelial oxidative stress is reversible with ARB, indicating RAS activation's role in early CVD risk in OSA.