期刊
HYPERTENSION
卷 42, 期 6, 页码 1067-1074出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/01.HYP.0000101686.98973.A3
关键词
hypertension, obesity; sleep apnea syndromes; sympathetic nervous system; insulin resistance
资金
- NATIONAL CENTER FOR RESEARCH RESOURCES [M01RR000585] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL070302, R01HL073211, R01HL065176, R01HL061560] Funding Source: NIH RePORTER
Obesity has a high and rising prevalence and represents a major public health problem. Obstructive sleep apnea ( OSA) is also common, affecting an estimated 15 million Americans, with a prevalence that is probably also rising as a consequence of increasing obesity. Epidemiologic data support a link between obesity and hypertension as well as between OSA and hypertension. For example, untreated OSA predisposes to an increased risk of new hypertension, and treatment of OSA lowers blood pressure, even during the daytime. Possible mechanisms whereby OSA may contribute to hypertension in obese individuals include sympathetic activation, hyperleptinemia, insulin resistance, elevated angiotensin II and aldosterone levels, oxidative and inflammatory stress, endothelial dysfunction, impaired baroreflex function, and perhaps by effects on renal function. The coexistence of OSA and obesity may have more widespread implications for cardiovascular control and dysfunction in obese individuals and may contribute to some of the clustering of abnormalities broadly defined as the metabolic syndrome. From the clinical and therapeutic perspectives, the presence of resistant hypertension and the absence of a nocturnal decrease in blood pressure in obese individuals should prompt the clinician to consider the diagnosis of OSA, especially if clinical symptoms suggestive of OSA ( such as poor sleep quality, witnessed apnea, excessive daytime somnolence, and so forth) are also present.
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