作者: T Kitazawa , S Kobayashi , K Horiuti , A V Somlyo , A P Somlyo
DOI: 10.1016/S0021-9258(18)83550-5
关键词: Inositol 、 Endocrinology 、 Phenylephrine 、 Carbachol 、 Phosphatidylinositol 、 Internal medicine 、 Muscle contraction 、 Biophysics 、 G protein 、 GTP' 、 Calcium 、 Biology
摘要: Abstract alpha-Adrenergic (phenylephrine) and muscarinic (carbachol) agonists inositol 1,4,5-trisphosphate caused calcium release contractions in smooth muscle strips permeabilized with Staphylococcus aureus alpha-toxin. The responses to phenylephrine carbachol required or were potentiated by added GTP could be inhibited GDP beta S. also increased the contractile response of portal vein cytoplasmic Ca2+. We conclude that while G-protein-coupled phosphatidylinositol cascade, through 1,4,5-trisphosphate-induced release, is a major mechanism pharmacomechanical coupling, second G-protein-mediated pathway modulates sensitivity regulatory proteins exists.