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We studied the influence of the alpha 2-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 alpha 2-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 less than 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 less than 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 alpha 2-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 alpha 2 receptors, then these receptors tonically suppress sympathetic outflow in humans.

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