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.
Original language | English |
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Pages (from-to) | 43-52 |
Number of pages | 10 |
Journal | Nature and Science of Sleep |
Volume | 5 |
DOIs | |
Publication status | Published - 2013 |
Externally published | Yes |
Bibliographical note
Copyright the Author(s) 2013. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.Keywords
- Ambulatory blood pressure
- Hypertension
- Intermittent hypoxia
- Obstructive sleep apnea
- Sympathetic activation