钙拮抗剂血管舒张作用的范围。

Blood vessels Pub Date : 1990-01-01 DOI:10.1159/000158825
G Fleckenstein-Grün, A Fleckenstein
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引用次数: 7

摘要

维拉帕米、硝苯地平和地尔硫卓类型的特异性钙拮抗剂已成为治疗心脏高运动性疾病和血管高张力(痉挛)的首选药物。钙拮抗剂血管扩张的具体机制是通过电生理、放射性核和机械测量证实的,测量对象包括不同类型的动脉血管,包括全身阻力血管和门静脉。结果表明,这些钙拮抗剂的血管扩张作用主要基于至少三个组成部分:(1)抑制钙携带膜电位的产生;(2)通过电位或受体操作的膜通道直接跨膜供应激活剂钙的减少;(3)间接干扰钙触发的细胞内钙释放,因为钙拮抗剂阻断少量触发钙的流入或产生细胞内钙储存的消耗。在任何情况下,如果钙拮抗剂被添加到缺钙介质中,跨膜钙供应被完全切断,收缩激活实际上就会停止。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Scope of vasodilatory effects of calcium antagonists.

Specific Ca antagonists of the verapamil, nifedipine, and diltiazem type have become the drugs of choice in the therapy of cardiac hyperkinetic disorders and of vascular hypertonicity (spasms). The specific mechanism of vasodilatation by Ca antagonists was substantiated by electrophysiological, radionuclear and mechanical measurements on rather different types of arterial vasculature, including the systemic resistance vessels, as well as on portal veins. The results indicate that the vasodilator efficacy of these Ca antagonists is mainly based on at least three components: (1) Suppression of the generation of Ca-carried membrane spike potentials; (2) decrease of direct transmembrane supply of activator Ca through potential- or receptor-operated membrane channels, and (3) interference with Ca-triggered intracellular Ca release in an indirect way, in that Ca antagonists block the influx of small amounts of trigger Ca or produce depletion of intracellular Ca stores. In any case, contractile activation practically ceases if transmembrane Ca supply is totally cut off upon addition of Ca antagonists to a Ca-deficient medium.

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