Somlyo A V, Somlyo A P
Department of Pathology and Molecular Physiology and Biological Physics, University of Virginia, Charlottesville 22908.
Adv Exp Med Biol. 1993;346:31-8. doi: 10.1007/978-1-4615-2946-0_4.
The two major modalities of pharmacomechanical coupling, inositol 1,4,5, trisphosphate induced Ca2+ release and modulation of Ca(2+)-sensitivity, are reviewed. Recent studies show that although changes in cytoplasmic Ca2+ play the major role in regulating smooth muscle contraction, agonists can also significantly affect the contractile state by modifying Ca(2+)-sensitivity. Inhibition of myosin light chain kinase or myosin light chain phosphatase leads to, respectively, desensitization or sensitization of the contractile apparatus to Ca2+. G-protein linked inhibition of myosin light chain phosphatase and Ca2+ release mediated by the phosphatidylinol cascade are the two major pharmacomechanical coupling mechanisms.
本文综述了药物机械偶联的两种主要方式，即肌醇1,4,5-三磷酸诱导的Ca2+释放和Ca(2+)敏感性的调节。最近的研究表明，虽然细胞质Ca2+的变化在调节平滑肌收缩中起主要作用，但激动剂也可通过改变Ca(2+)敏感性来显著影响收缩状态。抑制肌球蛋白轻链激酶或肌球蛋白轻链磷酸酶分别导致收缩装置对Ca2+的脱敏或致敏。G蛋白偶联的肌球蛋白轻链磷酸酶抑制和磷脂酰肌醇级联介导的Ca2+释放是两种主要的药物机械偶联机制。
