Tank Jens, Heusser Karsten, Diedrich André, Brychta Robert J, Luft Friedrich C, Jordan Jens
Franz Volhard Clinical Research Center, Medical Faculty of the Charité and HELIOS Klinikum, Berlin, Germany.
Hypertension. 2007 Nov;50(5):899-903. doi: 10.1161/HYPERTENSIONAHA.107.095984. Epub 2007 Sep 17.
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.
α-2肾上腺素能受体刺激可能通过激活副交感神经，显著增强压力反射介导的心动过缓。我们检验了内源性α-2肾上腺素能张力介导类似反应的假说。在10名健康男性（年龄：33±3岁；体重指数：24±1.3kg/m²）中，我们在摄入选择性α-2肾上腺素能受体拮抗剂育亨宾（20mg）或安慰剂后，测定了心率的压力反射控制和交感神经活动。测试以随机、双盲、交叉方式进行。我们测量了心率、肱动脉和手指血压以及肌肉交感神经活动。使用递增剂量的去氧肾上腺素和硝普钠输注（每分钟0.3、0.6、0.9、1.2和1.5μg/kg）来确定交感和副交感压力反射曲线。育亨宾使血浆去甲肾上腺素升高（50±38ng/L；P<0.05），而安慰剂使其无变化（2.2±7.6ng/L）。育亨宾使血压升高13±4/8±1mmHg，安慰剂使其升高6±2/3±1mmHg（P<0.01）。育亨宾使心率增加5±1次/分钟，而安慰剂使其无变化（P<0.01）。药物摄入90分钟后，育亨宾组和安慰剂组的静息肌肉交感神经活动相似。育亨宾使心率的压力反射控制降低（6毫秒/毫米汞柱对10毫秒/毫米汞柱；P<0.01），并重置为更高的血压和心率值。相比之下，育亨宾未改变交感压力反射曲线。育亨宾可能通过副交感机制选择性减弱正常血压年轻男性的压力反射心率控制。
