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(Hypertension. 1996;28:42-46.)
© 1996 American Heart Association, Inc.

Articles

Orthostatic Hypertension Due to Vascular Adrenergic Hypersensitivity

Neal L. Benowitz; Shoshana Zevin; Sandra Carlsen; Janet Wright; Morris Schambelan; Melvin Cheitlin

the Clinical Pharmacology (N.L.B., S.Z., S.C.), Endocrinology (M.S.), and Cardiology (J.W., M.C.) Units of the Medical Service, San Francisco General Hospital Medical Center, University of California, San Francisco.

Correspondence to Neal L. Benowitz, MD, Division of Clinical Pharmacology and Experimental Therapeutics, University of California, San Francisco, Box 1220, San Francisco, CA 94143-1220. E-mail nbeno@itsa.ucsf.edu.

Autoregulatory mechanisms ensure relatively small fluctuations of blood pressure with postural changes in healthy people. Although orthostatic hypotension is well recognized and commonly encountered, there are only a few reports of orthostatic hypertension. Most of the reported cases of orthostatic hypertension were related to excessive venous pooling, with an initial drop in cardiac output followed by overcompensation with an excessive release of catecholamines, or to nephroptosis with orthostatic activation of the renin-angiotensin system. We describe a 44-year-old woman with normal supine blood pressure and severe orthostatic hypertension who did not demonstrate an initial decrease in cardiac output and had normal plasma and urinary catecholamines and renin release. Pharmacological tests of autonomic nervous system function showed an increased pressor sensitivity to norepinephrine (11 to 14 times normal), normal sensitivity to isoproterenol, diminished baroreceptor reflex sensitivity, and exquisite sensitivity to -adrenergic blockers. This unusual case of orthostatic hypertension appears to be secondary to vascular adrenergic hypersensitivity.

Key Words: posture • hypertension, orthostatic • vascular resistance

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