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镉对离体牛蛙心房细胞等长收缩的阻滞作用。

Cadmium block of isometric contractions of isolated bullfrog atrial cells.

作者信息

Shepherd N, Kavaler F, Spielman W

机构信息

Department of Physiology, State University of New York, Brooklyn 11203.

出版信息

Am J Physiol. 1991 Feb;260(2 Pt 1):C249-58. doi: 10.1152/ajpcell.1991.260.2.C249.

Abstract

We studied the effect of cadmium, verapamil, and quinacrine on the force of contraction (Fp) of isolated, single, field-stimulated bullfrog atrial cells. All agents were applied or removed rapidly (t1/2 approximately 15 ms) to minimize intracellular concentration changes other than intracellular calcium concentration. Two components of twitch force were observed, one blocked by micromolar Cd2+ and the other by millimolar Cd2+. The two contributed about equally to the activation of the twitch. The "cadmium-sensitive" portion of force (that affected by [Cd] less than or equal to 100 microM) had a K1/2 approximately 1 microM, was identical in magnitude to, and not additive with, a "verapamil-sensitive" (10 microM) component of force, was most strongly affected by 50-ms pulses of Cd2+ when they were applied in the mechanical latent period, and was potentiated by catecholamines. The cadmium-insensitive portion of force was abolished by the removal of extracellular calcium and was greatly potentiated by quinacrine (3 or 10 microM), a blocker of Na-Ca exchange. The results are consistent with the idea that activating calcium enters the cell via both an inactivating cadmium-sensitive L-type channel and a noninactivating cadmium-insensitive mechanism that is not Na-Ca exchange and leaves the cell via Na-Ca exchange.

摘要

我们研究了镉、维拉帕米和喹吖因对离体单个场刺激牛蛙心房细胞收缩力(Fp)的影响。所有药物均快速施加或去除(半衰期约15毫秒),以尽量减少细胞内除钙浓度之外的浓度变化。观察到收缩力有两个成分,一个被微摩尔浓度的Cd2 +阻断,另一个被毫摩尔浓度的Cd2 +阻断。这两个成分对收缩激活的贡献大致相等。力的“镉敏感”部分(受[Cd]≤100微摩尔影响)的K1/2约为1微摩尔,其大小与力的“维拉帕米敏感”(10微摩尔)成分相同且无叠加性,当在机械潜伏期施加50毫秒的Cd2 +脉冲时受影响最强,并被儿茶酚胺增强。力的镉不敏感部分在去除细胞外钙后消失,并被钠钙交换阻滞剂喹吖因(3或10微摩尔)大大增强。结果与以下观点一致:激活钙通过一个失活的镉敏感L型通道和一个非失活的非钠钙交换的镉不敏感机制进入细胞,并通过钠钙交换离开细胞。

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