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Smooth muscle cell calcium activation mechanisms.

机译:平滑肌细胞钙激活机制。

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摘要

Smooth muscle cell (SMC) contraction is controlled by the Ca2+ and Rho kinase signalling pathways. While the SMC Rho kinase system seems to be reasonably constant, there is enormous variation with regard to the mechanisms responsible for generating Ca2+ signals. One way of dealing with this diversity is to consider how this system has been adapted to control different SMC functions. Phasic SMCs (vas deferens, uterus and bladder) rely on membrane depolarization to drive Ca2+ influx across the plasma membrane. This depolarization can be induced by neurotransmitters or through the operation of a membrane oscillator. Many tonic SMCs (vascular, airway and corpus cavernosum) are driven by a cytosolic Ca2+ oscillator that generates periodic pulses of Ca2+. A similar oscillator is present in pacemaker cells such as the interstitial cells of Cajal (ICCs) and atypical SMCs that control other tonic SMCs (gastrointestinal, urethra, ureter). The changes in membrane potential induced by these cytosolic oscillators does not drive contraction directly but it functions to couple together individual oscillators to provide the synchronization that is a characteristic feature of many tonic SMCs.
机译:平滑肌细胞(SMC)的收缩受Ca2 +和Rho激酶信号通路的控制。尽管SMC Rho激酶系统似乎相当恒定,但负责产生Ca2 +信号的机制却存在巨大差异。解决这种多样性的一种方法是考虑如何调整该系统以控制不同的SMC功能。阶段性SMC(输精管,子宫和膀胱)依靠膜去极化来驱动Ca2 +流入质膜。这种去极化可以由神经递质或通过膜振荡器的操作引起。许多补品SMC(血管,气道和海绵体)是由胞质Ca2 +振荡器驱动的,该振荡器会产生周期性的Ca2 +脉冲。起搏器细胞中存在类似的振荡器,例如Cajal的间质细胞(ICC)和控制其他补品SMC(胃肠道,尿道,输尿管)的非典型SMC。这些胞质振荡器诱发的膜电位变化不会直接驱动收缩,但会起到将各个振荡器耦合在一起的作用,以提供同步性,这是许多补品SMC的特征。

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