Influence of yohimbine on blood pressure, autonomic reflexes, and plasma catecholamines in humans

Abstract

We studied the influence of the a2-adrenoreceptor-blocking drug, yohimbine, on blood pressure, plasma norepinephrine, and other measures of autonomic function in normal male volunteers. These studies were designed to evaluate the role of o2-receptors in the tonic regulation of sympathetic outflow in humans. In a dose-ranging study, we found that yohimbine HCl (0.016-0.125 mg/kg) elicited dose-related rises in mean, systolic, and diastolic pressures. At the maximal dose used (0.125 mg/kg), respective increments in mean, systolic, and diastolic pressures were 14 ± 1 torr; 28 ± 3 torr; and 8 ± 1 torr (p < 0.01) (mean ± SE). NO significant changes in heart rate occurred. Associated with the rise in blood pressure were enhanced pressor and heart rate responses to the cold pressor, isometric handgrip, and Valsalva maneuvers. In a double-blind study, yohimbine (0.125 mg/kg bolus, 0.001 mg/kg/min infusion) induced a two-to-threefold rise in plasma norepinephrine (p < 0.01), without significantly altering plasma epinephrine or plasma renin activity. Ex vivo platelet aggregation in response to epinephrine was inhibited during yohimbine, showing that non-innervated a2-adrenoreceptors were inhibited. Central effects of yohimbine were evaluated through use of linear analog mood rating scales which showed a shift from calm toward excited ends of these scales. If yohimbine is acting through blockade of a2 receptors, then these receptors tonically suppress sympathetic outflow in humans. © 1983 American Heart Association, Inc.