Hai C M, Murphy R A
Division of Biology and Medicine, Brown University, Providence, Rhode Island 02912.
Am J Hypertens. 1990 Aug;3(8 Pt 2):235S-237S. doi: 10.1093/ajh/3.8.235.
A model is proposed to explain crossbridge regulation in smooth muscle and the latch state (high force with very low crossbridge cycling rates). The model predicts that low levels of [Ca2+] and myosin phosphorylation can induce high values of force. In this analysis we show that reductions in myosin light chain phosphatase activity make stress more proportional to phosphorylation, with abolition of the latch state. This may explain some of the differences in the phosphorylation dependence of force between intact and skinned smooth muscle.
提出了一个模型来解释平滑肌中的横桥调节和闩锁状态（横桥循环速率极低时产生高张力）。该模型预测，低水平的[Ca2+]和肌球蛋白磷酸化可诱导产生高张力值。在本分析中，我们表明肌球蛋白轻链磷酸酶活性降低会使张力与磷酸化更成比例，同时消除闩锁状态。这可能解释了完整平滑肌和去表皮平滑肌之间在张力的磷酸化依赖性方面的一些差异。
