Rembold C M, Murphy R A
Department of Internal Medicine, University of Virginia Health Science Center, Charlottesville 22908.
Am J Physiol. 1990 Aug;259(2 Pt 1):C251-7. doi: 10.1152/ajpcell.1990.259.2.C251.
Ca2+ concentration ([Ca2+])-dependent cross-bridge phosphorylation by myosin light chain kinase is postulated to be the primary regulator of stress development in smooth muscle. A four-state model of cross-bridge function, regulated only by [Ca2+]-dependent changes in myosin kinase activity, has been proposed to explain contraction and the latch state of smooth muscle (high force with reduced cross-bridge cycling and ATP consumption). A key test of this model is to determine whether changes in myoplasmic [Ca2+], per se, can quantitatively predict changes in myosin kinase activity, cross-bridge phosphorylation, and therefore force production. We find that changes in aequorin-estimated myoplasmic [Ca2+] can quantitatively predict the time course of phosphorylation and isometric stress production in response to stimulation with histamine and angiotensin II and during adenosine 3',5'-cyclic monophosphate-mediated relaxation when [Ca2+] is not changing rapidly. These results suggest that changes in myoplasmic [Ca2+] and activation of myosin light chain kinase may be sufficient to explain both contraction and relaxation of agonist stimulated swine carotid arterial smooth muscle.
肌球蛋白轻链激酶介导的Ca2+浓度（[Ca2+]）依赖性横桥磷酸化被认为是平滑肌应激发展的主要调节因子。有人提出了一种仅由肌球蛋白激酶活性的[Ca2+]依赖性变化调节的横桥功能四态模型，以解释平滑肌的收缩和闩锁状态（高张力伴随横桥循环和ATP消耗减少）。该模型的一个关键测试是确定肌浆[Ca2+]本身的变化是否能够定量预测肌球蛋白激酶活性、横桥磷酸化的变化，进而预测力的产生。我们发现，水母发光蛋白估计的肌浆[Ca2+]变化能够定量预测磷酸化的时间进程以及在组胺和血管紧张素II刺激时和[Ca2+]未快速变化的3',5'-环磷酸腺苷介导的舒张过程中的等长应激产生。这些结果表明，肌浆[Ca2+]的变化和肌球蛋白轻链激酶的激活可能足以解释激动剂刺激的猪颈动脉平滑肌的收缩和舒张。
