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Autonomic Dysfunction Clinic, Departments of Pharmacology and Medicine, Vanderbilt University School of Medicine, Nashville, TN.
Yohimbine is an 
2-adrenoreceptor antagonist that acts to enhance sympathetic nervous system discharge and potentiate sympathetically mediated cardiovascular reflex responses. We therefore assessed the ability of yohimbine to increase sympathoadrenal discharge and raise blood pressure (BP) in patients with autonomic failure characterized by profound orthostatic hypotension. Yohimbine 5 mg orally in eight seated patients significantly elevated mean systolic BP by 33 mm Hg from 136 ± 15 (mean ± SD) to a maximum of 169 ± 23 mm Hg (p < 0.01), mean diastolic BP by 16 mm Hg from 77 ± 9 to a maximum of 93 ± 15 mm Hg (p < 0.01), and mean heart rate (HR) by 10 beats per minute (BPM) from 68 ± 12 to a maximum of 781 17 BPM (p < 0.01). Plasma norepinephrine (NE) increased from 104 ± 71 to a maximum of 196 ± 182pg/ml(p < 0.05), but plasma epinephrine (E) did not increase significantly (31 ± 18 versus a maximum of 39 ± 21 pg/ml). In five patients given yohimbine 2.5 mg orally, BP, HR, NE, and E tended to increase, but the changes were not significant. Plasma yohimbine levels correlated significantly with the changes in mean arterial pressure (r = 0.61, p < 0.01). Yohimbine raises BP and HR in patients with autonomic failure. These effects are dose- and concentration-dependent and mediated through increased sympathetic discharge. Yohimbine may be useful in the treatment of orthostatic hypotension associated with autonomic failure. It is unique among current modes of therapy for this disorder in that it enhances discharge of the patient's own sympathetic system.
Address correspondence and reprint requests to Dr. Robertson, Autonomic Dysfunction Clinic, Departments of Pharmacology and Medicine, Vanderbilt University School of Medicine, Nashville, TN 37232.
Supported by GM 31304, HL-31419, and 5MO1RR0095 from the National Institutes of Health and a grant from the American Parkinson Disease Foundation, New York, NY. Dr. Onrot is supported by a research fellowship from the British Columbia Health Care Research Foundation, Vancouver, BC, Canada. Dr. Biaggioni is a Merck International Fellow, Dr. Hollister is a Burroughs Wellcome Fellow in Clinical Pharmacology and is supported by RF-00095. Dr. Robertson is a Burroughs Wellcome Scholar in Clinical Pharmacology.
Presented in part to the American Federation for Clinical Research, May 4, 1985.
Received April 2, 1986. Accepted for publication June 13, 1986
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