Allen B G, Walsh M P
Department of Medical Biochemistry, University of Calgary, Alberta, Canada.
Trends Biochem Sci. 1994 Sep;19(9):362-8. doi: 10.1016/0968-0004(94)90112-0.
The primary signal for smooth-muscle contraction is an increase in sarcoplasmic free Ca2+ concentration ([Ca2+]i). This triggers activation of calmodulin-dependent myosin light-chain kinase, which catalyses myosin phosphorylation, thereby activating crossbridge cycling and the development of force or contraction of the muscle cell. Restoration of resting [Ca2+]i deactivates the kinase; myosin is dephosphorylated by myosin light-chain phosphatase and the muscle relaxes. Recent evidence suggests that other signal-transduction pathways can modulate the contractile state of a smooth-muscle cell by affecting specific steps in the myosin phosphorylation-dephosphorylation mechanism.
平滑肌收缩的主要信号是肌浆游离钙离子浓度（[Ca2+]i）升高。这会触发钙调蛋白依赖性肌球蛋白轻链激酶的激活，该激酶催化肌球蛋白磷酸化，从而激活横桥循环并使肌肉细胞产生张力或收缩。静息[Ca2+]i的恢复会使激酶失活；肌球蛋白通过肌球蛋白轻链磷酸酶去磷酸化，肌肉随之松弛。最近的证据表明，其他信号转导途径可通过影响肌球蛋白磷酸化-去磷酸化机制中的特定步骤来调节平滑肌细胞的收缩状态。
