Inositol trisphosphate-induced calcium release and contraction in vascular smooth muscle.
Inositol trisphosphate-induced calcium release and contraction in vascular smooth muscle.
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DOI：
10.1073/pnas.82.15.5231
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发表时间：
1985-08
影响因子：
11.1
通讯作者：
A. Somlyo;M. Bond;A. Somlyo;A. Scarpa
中科院分区：
文献类型：
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作者：
A. Somlyo;M. Bond;A. Somlyo;A. Scarpa
三磷酸肌醇（InsP 3）可引起皂苷或毛地黄皂苷透化的兔主肺动脉平滑肌钙释放和张力发展。对InsP 3（0.5-30 μ M）的单次添加的这两种响应都是可重复的，并且在0.0-1.9 mM游离Mg 2+存在下发生。持续收缩由InsP 3诱导。用Ca 2+选择性电极测量的InsP 3释放的Ca的量也估计足以刺激完整平滑肌的收缩。线粒体氧化磷酸化抑制剂不影响钙释放。InsP 3敏感池对培养基中Ca ~（2+）的吸收具有ATP依赖性。目前的结果支持的假设，在平滑肌中，InsP 3是信使，或信使之一，参与递质诱导的（药理学）钙释放从肌浆网，这是细胞内钙存储先前确定为来源的主肺动脉去甲肾上腺素释放的钙。
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.