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Hypertension and obstructive sleep apnea

Authors Phillips CL, O’Driscoll DM

Received 7 February 2013

Accepted for publication 25 March 2013

Published 10 May 2013 Volume 2013:5 Pages 43—52


Checked for plagiarism Yes

Review by Single anonymous peer review

Peer reviewer comments 4

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Craig L Phillips,1–3 Denise M O'Driscoll4,5

Department of Respiratory and Sleep Medicine, Royal North Shore Hospital, Sydney, Australia; 2National Health and Medical Research Council Center for Integrated Research and Understanding of Sleep, Woolcock Institute of Medical Research, University of Sydney, Sydney, Australia; 3Discipline of Sleep Medicine, Sydney Medical School, University of Sydney, Sydney, Australia; 4Monash Lung and Sleep, Monash Medical Centre, Monash University, Melbourne, Australia; 5Department of Medicine, Southern Clinical School, Monash University, Melbourne, Australia

Abstract: Obstructive sleep apnea (OSA) is increasingly being recognized as a major health burden with strong focus on the associated cardiovascular risk. Studies from the last two decades have provided strong evidence for a causal role of OSA in the development of systemic hypertension. The acute physiological changes that occur during apnea promote nocturnal hypertension and may lead to the development of sustained daytime hypertension via the pathways of sympathetic activation, inflammation, oxidative stress, and endothelial dysfunction. This review will focus on the acute hemodynamic disturbances and associated intermittent hypoxia that characterize OSA and the potential pathophysiological mechanisms responsible for the development of hypertension in OSA. In addition the epidemiology of OSA and hypertension, as well as the role of treatment of OSA, in improving blood pressure control will be examined.

Keywords: obstructive sleep apnea, hypertension, intermittent hypoxia, ambulatory blood pressure, sympathetic activation

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