穿孔哺乳动物心肌细胞中钙敏感性的调节。
Regulation of calcium sensitivity in perforated mammalian cardiac cells.
作者信息
Weisberg A, McClellan G, Tucker M, Lin L E, Winegrad S
出版信息
J Gen Physiol. 1983 Feb;81(2):195-211. doi: 10.1085/jgp.81.2.195.
Abstract
Sarcolemmal perforations can be produced in bundles of rat right ventricular cells by either perfusion of the heart or soaking of the bundles with a solution containing 10 mM EGTA. All cells are affected and lose approximately 40% of the surface membrane. In these cells it is possible to show cAMP regulation of contractility (maximum Ca-activated force) without cAMP regulation of Ca sensitivity (pCa for 50% of maximum Ca-activated force). Therefore, the target molecule for cAMP is different for the two regulatory systems. Both regulatory systems can be slowly washed out of the cell by 10 mM EGTA solution but not by relaxing or contraction solutions. A model for regulation of Ca sensitivity is proposed.
摘要
通过灌注心脏或将肌束浸泡在含有10 mM乙二醇双四乙酸（EGTA）的溶液中，可以在大鼠右心室肌束中产生肌膜穿孔。所有细胞均受影响，表面膜损失约40%。在这些细胞中，可以显示环磷酸腺苷（cAMP）对收缩性（最大钙激活力）的调节，而不存在cAMP对钙敏感性（最大钙激活力的50%时的pCa）的调节。因此，两种调节系统中cAMP的靶分子不同。两种调节系统都可以被10 mM EGTA溶液缓慢从细胞中洗脱，但不能被舒张或收缩溶液洗脱。本文提出了一种钙敏感性调节模型。
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