肌醇三磷酸诱导的血管平滑肌钙释放与收缩
Inositol trisphosphate-induced calcium release and contraction in vascular smooth muscle.
作者信息
Somlyo A V, Bond M, Somlyo A P, Scarpa A
出版信息
Proc Natl Acad Sci U S A. 1985 Aug;82(15):5231-5. doi: 10.1073/pnas.82.15.5231.
Abstract
Inositol 1,4,5-trisphosphate (InsP3) caused Ca release and tension development in rabbit main pulmonary artery smooth muscle permeabilized with saponin or digitonin. Both of these responses to single additions of InsP3 (0.5-30 microM) were repeatable and occurred in the presence of 0.0-1.9 mM free Mg2+. Sustained contractions were induced by InsP3. The amount of Ca released by InsP3, measured with a Ca2+-selective electrode, was also estimated to be sufficient to stimulate contraction in intact smooth muscle. Ca release was not influenced by inhibitors of mitochondrial oxidative phosphorylation. The uptake of Ca2+ from the medium into the InsP3-sensitive pool was ATP-dependent. The present results support the hypothesis that, in smooth muscle, InsP3 is the messenger, or one of the messengers, involved in transmitter-induced (pharmacomechanical) Ca release from the sarcoplasmic reticulum, which is the intracellular Ca store identified previously as the source of Ca released by norepinephrine in main pulmonary artery.
摘要
肌醇1,4,5 -三磷酸（InsP3）可使经皂角苷或洋地黄皂苷通透处理的兔主肺动脉平滑肌释放钙离子并产生张力。对单次添加InsP3（0.5 - 30微摩尔）的这两种反应均可重复出现，且在游离镁离子浓度为0.0 - 1.9毫摩尔的情况下发生。InsP3可诱导持续性收缩。用钙离子选择性电极测得的InsP3释放的钙量，据估计也足以刺激完整平滑肌收缩。线粒体氧化磷酸化抑制剂不影响钙的释放。钙离子从培养基进入InsP3敏感池的摄取过程依赖于ATP。目前的结果支持这样一种假说，即在平滑肌中，InsP3是参与递质诱导（药物 - 机械性）从肌浆网释放钙离子的信使或信使之一，肌浆网是先前确定的主肺动脉中去甲肾上腺素释放钙离子的细胞内钙库。
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