Lee Cheng-Han, Poburko Damon, Kuo Kuo-Hsing, Seow Chun Yong, van Breemen Cornelis
The iCAPTURE Center, University of British Columbia, St. Paul's Hospital, Vancouver, British Columbia, V6Z 1Y6, Canada.
Am J Physiol Heart Circ Physiol. 2002 May;282(5):H1571-83. doi: 10.1152/ajpheart.01035.2001.
Vascular smooth muscle shows both plasticity and heterogeneity with respect to Ca(2+) signaling. Physiological perturbations in cytoplasmic Ca(2+) concentration (Ca(2+)) may take the form of a uniform maintained rise, a transient uniform Ca(2+) elevation, a transient localized rise in Ca(2+) (also known as spark and puff), a transient propagated wave of localized Ca(2+) elevation (Ca(2+) wave), recurring asynchronous Ca(2+) waves, or recurring synchronized Ca(2+) waves dependent on the type of blood vessel and the nature of stimulation. In this overview, evidence is presented which demonstrates that interactions of ion transporters located in the membranes of the cell, sarcoplasmic reticulum, and mitochondria form the basis of this plasticity of Ca(2+) signaling. We focus in particular on how the junctional complexes of plasmalemma and superficial sarcoplasmic reticulum, through the generation of local cytoplasmic Ca(2+) gradients, maintain Ca(2+) oscillations, couple these to either contraction or relaxation, and promote Ca(2+) cycling during homeostasis.
血管平滑肌在钙信号传导方面表现出可塑性和异质性。细胞质钙浓度([Ca²⁺]i)的生理扰动可能表现为持续均匀升高、短暂均匀的[Ca²⁺]i升高、[Ca²⁺]i的短暂局部升高(也称为火花和阵发)、局部[Ca²⁺]i升高的短暂传播波(钙波)、反复出现的异步钙波或反复出现的同步钙波,这取决于血管类型和刺激性质。在本综述中,我们提供的证据表明,位于细胞膜、肌浆网和线粒体膜上的离子转运体之间的相互作用构成了钙信号传导这种可塑性的基础。我们特别关注质膜和浅表肌浆网的连接复合体如何通过产生局部细胞质钙梯度来维持[Ca²⁺]i振荡,将这些振荡与收缩或舒张耦合,并在稳态期间促进钙循环。