MECHANISM OF CALCIUM-CHANNEL BLOCKADE BY VERAPAMIL, D600, DILTIAZEM AND NITRENDIPINE IN SINGLE DIALYZED HEART-CELLS
MECHANISM OF CALCIUM-CHANNEL BLOCKADE BY VERAPAMIL, D600, DILTIAZEM AND NITRENDIPINE IN SINGLE DIALYZED HEART-CELLS
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DOI：
10.1038/302790a0
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发表时间：
1983-01-01
期刊：
影响因子：
64.8
通讯作者：
TSIEN, RW
中科院分区：
文献类型：
--
作者：
LEE, KS;TSIEN, RW
钙内流的有机抑制剂阻止向外和向内通过心脏钙通道的电流，但不减缓电流的激活。尽管通过提高外部Ca或Ba浓度可以拮抗阻滞，但渗透阳离子的竞争效应并不发生在无机阻滞剂作用的相同阳离子结合位点。有机药物表现出不同程度的使用依赖性阻滞，部分原因是开放通道的阻滞。尼群地平阻断钙电流所需的剂量比放射性配体结合到分离膜所需的剂量高100倍。[实验是用从豚鼠心室分离的单个心脏细胞进行的。]
Organic inhibitors of Ca influx prevent outward as well as inward current through cardiac Ca channels but do not slow current activation. Although block is antagonized by raising external Ca or Ba concentrations, the competitive effect of permeant cations does not occur at the same cation binding site at which inorganic blockers act. Organic drugs show varying degrees of use-dependent block, due in part to blockade of open channels. Nitrendipine blockade of Ca currents requires doses > 100-fold higher than expected from radioligand binding to isolated membranes. [Experiments were carried out with single isolated heart cells isolated from guinea pig ventricles.].