Intermittent Hypoxia Increases Arterial Blood Pressure in Humans Through a Renin-Angiotensin System–Dependent Mechanism

Intermittent hypoxia (IH) is believed to contribute to the pathogenesis of hypertension in obstructive sleep apnea through mechanisms that include activation of the renin-angiotensin system. The objective of this study was to assess the role of the type I angiotensin II receptor in mediating an incr...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2010-09, Vol.56 (3), p.369-377
Main Authors: Foster, Glen E, Hanly, Patrick J, Ahmed, Sofia B, Beaudin, Andrew E, Pialoux, Vincent, Poulin, Marc J
Format: Article
Language:English
Subjects:
Adult
Analysis of Variance
Angiotensin II Type 1 Receptor Blockers - pharmacology
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Pressure - drug effects
Blood Pressure - physiology
Cardiology. Vascular system
Cerebrovascular Circulation - drug effects
Cerebrovascular Circulation - physiology
Cross-Over Studies
Double-Blind Method
Endocrine kidney. Renin-angiotensin-aldosterone system
Fundamental and applied biological sciences. Psychology
Humans
Hypoxia - physiopathology
Life Sciences
Losartan - pharmacology
Male
Medical sciences
Receptor, Angiotensin, Type 1 - physiology
Renin-Angiotensin System - drug effects
Renin-Angiotensin System - physiology
Vertebrates: endocrinology
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Summary:Intermittent hypoxia (IH) is believed to contribute to the pathogenesis of hypertension in obstructive sleep apnea through mechanisms that include activation of the renin-angiotensin system. The objective of this study was to assess the role of the type I angiotensin II receptor in mediating an increase in arterial pressure associated with a single 6-hour IH exposure. Using a double-blind, placebo-controlled, randomized, crossover study design, we exposed 9 healthy male subjects to sham IH, IH with placebo medication, and IH with the type I angiotensin II receptor antagonist losartan. We measured blood pressure, cerebral blood flow, and ventilation at baseline and after exposure to 6 hours of IH. An acute isocapnic hypoxia experimental protocol was conducted immediately before and after exposure to IH. IH with placebo increased resting mean arterial pressure by 7.9±1.6 mm Hg, but mean arterial pressure did not increase with sham IH (1.9±1.5 mm Hg) or with losartan IH (−0.2±2.4 mm Hg; P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.110.152108