Smooth muscle: excitation-contraction coupling, contractile regulation, and the cross-bridge cycle.
Smooth muscle: excitation-contraction coupling, contractile regulation, and the cross-bridge cycle.
复制标题
DOI：
10.1111/j.1530-0277.1994.tb00893.x
复制
发表时间：
1994-02
期刊：
影响因子：
--
通讯作者：
A. Somlyo;A. Somlyo
中科院分区：
文献类型：
--
作者：
A. Somlyo;A. Somlyo
平滑肌中的兴奋-兴奋偶联通过两个主要途径进行：机电偶联和药物力学偶联。药物力学偶联是一系列机制的集合，这些机制可以通过释放细胞内Ca 2+、调节（降低或增加）收缩调节的Ca 2+敏感性以及通过配体门控的非选择性通道适度增加Ca 2+内流，独立于膜电位的变化而激活或抑制平滑肌（综述见参考文献3）。与通过去极化激活的电压操作通道相反，通过配体门控通道的Ca 2+内流通过为阳离子内流提供电驱动力的负电位增强。然而，这两种机制，机电和药物机械，可以同时运作。表面膜电位对兴奋性激动剂的反应是有些可变的，因为这些电效应取决于阳离子和阴离子渗透性的相对变化，以及给定平滑肌中渗透离子的预先存在的平衡电位。例如，由于平滑肌中的C1-平衡电位比静息膜电位更正，K+平衡电位比静息膜电位更负，激动剂或（释放的）Ca 2+激活C1-通道将导致去极化，而激活K+通道将导致超极化。膜电位也可能受到生电泵（变化）的影响，最近人们认识到，膜电位还可能受到激动素释放的“信使”（如Ca和花生四烯酸）对离子通道的次级效应的影响。
XCITATION-CONTRACTION coupling in smooth E muscle proceeds through two major pathways: electromechanical coupling and pharmacomechanical coupling. Pharmacomechanical coupling is the assemblage of mechanisms that can activate or inactivate smooth muscle independently of changes in membrane potential through the release of intracellular Ca2+ and through modulation (decrease or increase) in the Ca2+ sensitivity of the contractile regulatory and through moderate increases in Ca” influx through ligand-gated, nonselective channels (reviewed in ref. 3). In contrast to the voltageoperated channels that are activated by depolarization, Ca2+ influx through ligand-gated channels is enhanced by negative potentials that provide the electrical driving force for cation influx. However, the two mechanisms, electromechanical and pharmacomechanical, can operate simultaneously.’The response of the surface membrane potential to excitatory agonists is somewhat variable, because these electrical effects depend on the relative changes in cation and anion permeabilities, as well as on the preexisting equilibrium potentials of the permeant ions in a given smooth muscle. For example, because the C1-equilibrium potential in smooth muscle is more positive and the K+ equilibrium potential is more negative than the resting membrane potential, the activation of the C1-channels by agonists or by (released) Ca2+ will lead to depolarization, whereas activation of K+ channels will cause hyperpolarization. The membrane potential may also be affected by (changes in) electrogenic pumps and, as realized more recently, by the secondary effects, on ion channels, of “messengers”(eg, Ca” and arachidonic acid) released by the agoni~ ts.~