Mancia G, Parati G, Grassi G, Pomidossi G, Giannattasio C, Casadei R, Groppelli A, Saino A, Gregorini L, Perondi R
Istituto di Clinica Medica Generale e Terapia Medica, Università di Milano, Italy.
J Hypertens Suppl. 1987 Dec;5(4):S49-55. doi: 10.1097/00004872-198712004-00009.
Data from animals and from man suggest that calcium antagonists interfere with alpha-adrenergic receptors and that this mechanism may be responsible for some of the vasodilation induced by these drugs. However, alpha-adrenergic receptors play a primary role in baroreceptor regulation of the cardiovascular system and blood pressure homeostasis, which might therefore be adversely affected by calcium antagonist treatment. We addressed this question in 14 essential hypertensives studied before treatment, 1 h after 20 mg oral nitrendipine and 5-7 days after daily administration of 20 mg oral nitrendipine. Blood pressure was measured by an intra-arterial catheter, heart rate by an electrocardiogram, cardiac output by thermodilution and forearm blood flow by venous occlusion plethysmography. Total peripheral and forearm vascular resistances were calculated by dividing mean blood pressure by blood flow values. Plasma norepinephrine was also measured (high performance liquid chromatography) in blood taken from the right atrium. Compared with the pretreatment values, acute nitrendipine administration caused a fall in resting blood pressure, an increase in the resting heart rate and cardiac output, and a fall in resting peripheral and forearm vascular resistance. The resting hypotension and vasodilation were also evident during the prolonged nitrendipine administration, which was, however, accompanied by much less resting cardiac stimulation than that observed in the acute condition. Baroreceptor control of the heart rate (vasoactive drug method) was similar before and after acute and prolonged nitrendipine treatment. This was also the case for carotid baroreceptor control of blood pressure (neck chamber technique) and for control of forearm vascular resistance as exerted by receptors in the cardiopulmonary region (lower-body negative-pressure and passive leg-raising techniques).(ABSTRACT TRUNCATED AT 250 WORDS)
来自动物和人类的数据表明，钙拮抗剂会干扰α-肾上腺素能受体，且这一机制可能是这些药物所致某些血管舒张的原因。然而，α-肾上腺素能受体在心血管系统的压力感受器调节和血压稳态中起主要作用，因此钙拮抗剂治疗可能会对其产生不利影响。我们对14例原发性高血压患者进行了研究，分别在治疗前、口服20 mg尼群地平1小时后以及每日口服20 mg尼群地平5 - 7天后进行观察。通过动脉内导管测量血压，通过心电图测量心率，通过热稀释法测量心输出量，通过静脉阻断体积描记法测量前臂血流量。通过平均血压除以血流量值计算总外周血管阻力和前臂血管阻力。还采用高效液相色谱法测量了取自右心房血液中的血浆去甲肾上腺素。与治疗前的值相比，急性给予尼群地平导致静息血压下降、静息心率和心输出量增加，以及静息外周血管阻力和前臂血管阻力下降。在长期给予尼群地平期间，静息性低血压和血管舒张也很明显，然而，与急性给药时相比，此时静息时心脏的刺激要小得多。急性和长期尼群地平治疗前后，压力感受器对心率的控制（血管活性药物法）相似。颈动脉压力感受器对血压的控制（颈室技术）以及心肺区域受体对前臂血管阻力的控制（下体负压和被动抬腿技术）也是如此。（摘要截选于250词）
