de Leeuw P W, Blok W L, van Es P N, Tchang P T, Birkenhäger W H
Arch Mal Coeur Vaiss. 1985 Nov;78 Spec No:51-4.
Interference with the function of the sympathetic nervous system is one of the possible mechanisms whereby calcium-antagonists may lower blood pressure. We have studied the effects of one of those drugs (verapamil) on blood pressure and basal levels of catecholamines. The hypotensive response appeared to be associated with a small insignificant rise in noradrenaline and a significant fall in adrenaline. To explore the role of extracellular calcium we infused calcium gluconate before and during treatment with verapamil. Calcium had only little effect on plasma noradrenaline, but markedly stimulated adrenaline. The latter was not affected by verapamil when given intravenously, but clearly blunted after a period of oral treatment with verapamil. Noradrenaline release was enhanced by calcium during administration of verapamil. It is concluded that extracellular calcium may be involved in the secretion of adrenaline and that this requires transmembrane calcium influx. Perhaps a reduction in circulating adrenaline contributes to the blood pressure lowering effects of verapamil.
干扰交感神经系统功能是钙拮抗剂降低血压的可能机制之一。我们研究了其中一种药物（维拉帕米）对血压和儿茶酚胺基础水平的影响。降压反应似乎与去甲肾上腺素的小幅无显著升高以及肾上腺素的显著下降有关。为了探究细胞外钙的作用，我们在维拉帕米治疗前和治疗期间输注葡萄糖酸钙。钙对血浆去甲肾上腺素影响很小，但能显著刺激肾上腺素。静脉注射维拉帕米时，肾上腺素不受影响，但在口服维拉帕米一段时间后明显减弱。在维拉帕米给药期间，钙可增强去甲肾上腺素的释放。结论是细胞外钙可能参与肾上腺素的分泌，且这需要跨膜钙内流。或许循环中肾上腺素的减少有助于维拉帕米的降压作用。
