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皮肤化肌纤维中兴奋-收缩偶联的机制。

Mechanisms of excitation-contraction coupling in skinned muscle fibers.

作者信息

Donaldson S K

机构信息

Department of Physiology, School of Medicine, University of Minnesota, Minneapolis 55455.

出版信息

Med Sci Sports Exerc. 1989 Aug;21(4):411-7.

PMID:2674592
Abstract

Although the mechanisms underlying most aspects of excitation-contraction (EC) coupling in skeletal muscle are well understood, a very basic step, that of communication between the transverse tubule (TT) region of the plasmalemma and the terminal cisternae of the sarcoplasmic reticulum (SR), has not been elucidated. Several types of TT to SR communication have been proposed, including electrical, chemical, and mechanical coupling. Current evidence supports a combination of the latter two. Studies of single rabbit skeletal muscle fibers, skinned by peeling the sarcolemma, demonstrate that a chemical stimulus for SR Ca2+ release, inositol trisphosphate (InsP3), could play a role in skeletal EC coupling. InsP3 appears to open the same SR Ca2+ channel that is activated by caffeine, Ca2+, and depolarization of TTs; all of these stimuli are inhibited by the SR Ca2+ channel blocker ruthenium red.

摘要

尽管骨骼肌兴奋-收缩(EC)偶联大多数方面的潜在机制已得到充分理解,但一个非常基本的步骤,即质膜横小管(TT)区域与肌浆网(SR)终末池之间的信号传递,尚未阐明。已经提出了几种类型的TT与SR之间的信号传递方式,包括电偶联、化学偶联和机械偶联。目前的证据支持后两种方式的结合。对通过剥除肌膜而剥制的单个兔骨骼肌纤维的研究表明,一种用于SR Ca2+释放的化学刺激物,即肌醇三磷酸(InsP3),可能在骨骼肌EC偶联中起作用。InsP3似乎打开了与被咖啡因、Ca2+和TT去极化激活的相同的SR Ca2+通道;所有这些刺激都被SR Ca2+通道阻滞剂钌红抑制。

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