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(Hypertension. 2004;43:518.)
© 2004 American Heart Association, Inc.

Hypertension Grand Rounds

Resistant Hypertension, Obesity, Sleep Apnea, and Aldosterone

Theory and Therapy

From William S. Middleton Memorial Veterans Hospital (T.L.G.) and Departments of Medicine and Pharmacology (T.L.G.), University of Wisconsin, Madison; and Vascular Biology and Hypertension Program (D.A.C.), University of Alabama at Birmingham.

Correspondence to Theodore L. Goodfriend, Research Service, William S. Middleton Memorial Veterans Hospital, 2500 Overlook Terrace, Madison, WI 53705. E-mail tgoodfri{at}facstaff.wisc.edu

Hypertension resistant to 2 antihypertensive drugs is more common among obese patients than among lean patients. The case we describe and the observations we report suggest that refractoriness among obese hypertensives is frequently caused by obstructive sleep apnea and/or inappropriately high plasma aldosterone levels. In other words, obese hypertensives may have sleep apnea, obese hypertensives without sleep apnea may have inappropriately elevated levels of plasma aldosterone, and a surprising number of obese patients with sleep apnea also have elevated levels of aldosterone. The mechanisms by which obesity and obstructive sleep apnea increase aldosterone levels and raise blood pressure are not understood, but sympathetic nervous system activation and production of nonclassical adrenal stimuli are two possibilities. Obstructive sleep apnea can be detected with a careful history and various sleep studies. Inappropriately elevated aldosterone levels can be detected by measuring the ratio of plasma aldosterone concentration to plasma renin activity. Successful treatment of these resistant hypertensives often can be achieved by devices that provide positive pressure to the upper airway to correct obstructive sleep apnea and by incorporating an aldosterone antagonist in the therapeutic regimen.

Key Words: obesity • aldosterone • sleep apnea • hypertension • fatty acids • renin