Alpha-2 adrenoreceptor stimulation profoundly augments baroreflex-mediated
bradycardia presumably through parasympathetic activation. We tested the hypothesis that endogenous alpha-2
adrenergic tone mediates a similar response. In 10 healthy men (age: 33+/-3 years; body mass index: 24+/-1.3 kg/m(2)), we determined baroreflex control of heart rate and sympathetic traffic after ingestion of the selective alpha-2
adrenoceptor antagonist
yohimbine (20 mg) or placebo. Testing was conducted in a randomized, double-blind, crossover fashion. We measured heart rate, brachial and finger blood pressure, and muscle sympathetic nerve activity. Sympathetic and parasympathetic baroreflex curves were determined using incremental
phenylephrine and
nitroprusside infusions (0.3, 0.6, 0.9, 1.2, and 1.5 microg/kg per minute). Plasma
norepinephrine increased with
yohimbine (50+/-38 ng/L; P<0.05) and was unchanged with placebo (2.2+/-7.6 ng/L). Blood pressure increased 13+/-4/8+/-1 mm Hg with
yohimbine and 6+/-2/3+/-1 mm Hg with placebo (P<0.01). HR increased 5+/-1 bpm with
yohimbine but did not change with placebo (P<0.01). Ninety minutes after
drug ingestion, resting muscle sympathetic nerve activity was similar with
yohimbine and with placebo. Baroreflex control of heart rate was decreased with
yohimbine (6 ms/mm Hg versus 10 ms/mm Hg; P<0.01) and reset to higher blood pressure and heart rate values. In contrast,
yohimbine did not alter the sympathetic baroreflex curve.
Yohimbine selectively attenuates baroreflex heart rate control in normotensive young men possibly through parasympathetic mechanisms.