Akata Takashi
Department of Anesthesiology and Critical Care Medicine, Faculty of Medicine, Kyushu University, 3-1-1 Maidashi, Fukuoka 812-8582, Japan.
J Anesth. 2007;21(2):232-42. doi: 10.1007/s00540-006-0488-4. Epub 2007 May 30.
Understanding the physiological mechanisms regulating vascular tone would lead to better circulatory management during general anesthesia. This two-part review provides an overview of current knowledge about the cellular and molecular mechanisms regulating the contractile state of vascular smooth muscle cells (i.e., vascular tone). The first part reviews basic mechanisms controlling the cytosolic Ca2+ concentration in vascular smooth muscle cells, and the Ca2+-dependent regulation of vascular tone. This second part reviews the regulatory mechanisms modulating Ca2+ mobilization and/or myofilament Ca2+ sensitivity in vascular smooth muscle cells-including Rho/Rho kinase, protein kinase C, arachidonic acid, Ca2+/calmodulin-dependent protein kinase II, caldesmon, calponin, mitogen-activated protein kinases, tyrosine kinases, cyclic nucleotides, Cl- channels, and K+ channels.
了解调节血管张力的生理机制将有助于在全身麻醉期间实现更好的循环管理。这篇分两部分的综述概述了目前关于调节血管平滑肌细胞收缩状态（即血管张力）的细胞和分子机制的知识。第一部分回顾了控制血管平滑肌细胞胞质Ca2+浓度的基本机制，以及Ca2+依赖性血管张力调节。第二部分回顾了调节血管平滑肌细胞中Ca2+动员和/或肌丝Ca2+敏感性的调节机制，包括Rho/Rho激酶、蛋白激酶C、花生四烯酸、Ca2+/钙调蛋白依赖性蛋白激酶II、钙调素、钙结合蛋白、丝裂原活化蛋白激酶、酪氨酸激酶、环核苷酸、Cl-通道和K+通道。
