Effects of Bromocriptine on Cardiovascular Regulation in Healthy Humans

Abstract Bromocriptine, a dopamine agonist with central nervous system actions, may reduce sympathetic nervous system activity. We tested this hypothesis by measuring arterial blood pressure, central venous pressure, heart rate, muscle sympathetic nerve activity, and forearm blood flow before and after unloading the arterial baroreceptors with sodium nitroprusside (0.5 to 1.5 mcg/kg per minute IV), before and after unloading the cardiopulmonary baroreceptors with incremental lower body negative pressure (0 to −15 mm Hg), and before and after immersion of the hand in ice-cold water for 2 minutes (cold pressor test). After obtaining basal responses to provocative maneuvers, we gave 20 healthy subjects either 5 mg oral bromocriptine (n=10) or placebo (n=10) in a randomized, double-blind fashion. Bromocriptine did not affect resting mean arterial pressure, heart rate, or forearm blood flow. Bromocriptine decreased resting central venous pressure by 1.2 mm Hg ( P <.05) and tended to increase total integrated muscle sympathetic nerve activity (from 151±44 to 212±82 U/min, P =NS). The reflex increases in muscle sympathetic nerve activity to nitroprusside infusion and lower body negative pressure were unchanged by bromocriptine; however, vascular responsiveness to both maneuvers was impaired after bromocriptine administration compared with control. Without bromocriptine, the reflex increase in muscle sympathetic nerve activity after nitroprusside-induced hypotension maintained forearm blood flow at a constant level, whereas with bromocriptine the forearm blood flow increased from 1.9±0.3 to 2.8±0.6 mL/min per 100 mL ( P <.05). Similarly, the forearm blood flow response to lower body negative pressure at −15 mm Hg was decreased with bromocriptine (+0.0±0.4 mL/min per 100 mL) compared with control values (−0.4±0.3 mL/min per 100 mL, P <.05). Responses to the cold pressor test were not altered by bromocriptine. We conclude that bromocriptine inhibits catecholamine release in peripheral nerves. However, we were unable to substantiate a central effect of bromocriptine on either sympathetic outflow or baroreflex sensitivity.