毒胡萝卜素对豚鼠心脏单个心肌细胞肌浆网Ca2+含量及收缩的影响。

The effect of thapsigargin on sarcoplasmic reticulum Ca2+ content and contractions in single myocytes of guinea-pig heart.

作者信息

Lewartowski B, Wolska B M

机构信息

Department of Clinical Physiology, Medical Centre of Postgraduate Education, Warsaw, Poland.

出版信息

J Mol Cell Cardiol. 1993 Jan;25(1):23-9. doi: 10.1006/jmcc.1993.1004.

DOI:10.1006/jmcc.1993.1004

PMID:8441178

Abstract

Contractures initiated by 1 s superfusion of single myocytes of guinea-pig heart with 10 mM caffeine were used as a relative index of the SR Ca2+ content. Thapsigargin (Tg) in concentration 2 x 10(-7) M completely blocked Ca2+ uptake during electrical stimulation by the SR from which Ca2+ has been previously depleted by caffeine. Tg did not affect the SR Ca2+ content in the resting myocytes and did not block release of the SR Ca2+ during electrically stimulated contractions (ESCs). It is concluded that in guinea-pig myocytes Tg affects SR Ca2+ by selective blocking the SR Ca2+ uptake. The amplitude of steady state ESCs dropped to 68 +/- 5.4% (S.D., n = 20) of that of the pre-Tg control. Time to peak contraction increased from 454 +/- 82.4 ms to 820 +/- 157.4 ms and time of relaxation increased from 368 +/- 90.8 ms to 474 +/- 87 ms after the SR Ca2+ has been depleted by Tg. Rest decay of contractions, post-extrasystolic potentiation and post-rest potentiation were inhibited.

摘要

将豚鼠心脏单个心肌细胞用10 mM咖啡因超灌流1秒引发的挛缩用作肌浆网Ca2+含量的相对指标。浓度为2×10(-7) M的毒胡萝卜素（Tg）完全阻断了肌浆网在电刺激期间的Ca2+摄取，此前Ca2+已被咖啡因耗尽。Tg不影响静息心肌细胞中的肌浆网Ca2+含量，也不阻断电刺激收缩（ESC）期间肌浆网Ca2+的释放。得出结论，在豚鼠心肌细胞中，Tg通过选择性阻断肌浆网Ca2+摄取来影响肌浆网Ca2+。稳态ESC的幅度降至Tg处理前对照的68±5.4%（标准差，n = 20）。在肌浆网Ca2+被Tg耗尽后，收缩峰值时间从454±82.4毫秒增加到820±157.4毫秒，舒张时间从368±90.8毫秒增加到474±87毫秒。收缩的静息衰减、期外收缩后增强和静息后增强均受到抑制。