Hirata M, Kukita M, Sasaguri T, Suematsu E, Hashimoto T, Koga T
J Biochem. 1985 Jun;97(6):1575-82. doi: 10.1093/oxfordjournals.jbchem.a135214.
Inositol 1,4,5-trisphosphate (InsP3) releases Ca2+ from the non-mitochondrial Ca2+ store site of various types of cells. To study the mechanisms of the Ca2+ release from the store site, the effect of InsP3 on the passive Ca2+ release and influx, and the active Ca2+ uptake in the presence of oxalate, was examined using saponin-treated guinea pig peritoneal macrophages. InsP3 stimulated the passive Ca2+ release and influx. Although InsP3 slightly inhibited the active Ca2+ uptake in the presence of oxalate, it seems unlikely that the Ca2+ release by this agent is caused by the inhibition of the Ca2+ uptake, because the addition of apyrase or hexokinase (which removes ATP within 30 s, so that no more Ca2+ can be accumulated) or vanadate (which inhibits the Ca2+ uptake) resulted in very slow release of Ca2+. These results suggest that the Ca2+ permeability of the Ca2+ store membrane is increased by InsP3. InsP3 did not cause an increase in the Ca2+ permeability of phospholipid vesicles (liposomes), indicating that this agent may bring about Ca2+ release by a specific effect on the physiologically relevant Ca2+ channels or carriers in the non-mitochondrial Ca2+ store site. The passive Ca2+ release by InsP3 was enhanced by ATP and an unhydrolyzable ATP analogue, 5'-adenylyimidodiphosphate, but not by ADP or AMP. The passive Ca2+ release by InsP3 was observed even at 0 degree C.
肌醇1,4,5 - 三磷酸（InsP3）可从各类细胞的非线粒体钙储存位点释放Ca2+。为研究钙从储存位点释放的机制，我们使用皂素处理的豚鼠腹腔巨噬细胞，检测了InsP3对被动钙释放、内流以及在草酸盐存在下主动钙摄取的影响。InsP3刺激了被动钙释放和内流。尽管InsP3在草酸盐存在时略微抑制了主动钙摄取，但该试剂引起的钙释放似乎不太可能是由钙摄取的抑制所致，因为添加腺苷三磷酸双磷酸酶或己糖激酶（可在30秒内去除ATP，从而无法再积累更多Ca2+）或钒酸盐（抑制钙摄取）导致钙释放非常缓慢。这些结果表明，InsP3增加了钙储存膜的钙通透性。InsP3并未导致磷脂囊泡（脂质体）的钙通透性增加，这表明该试剂可能通过对非线粒体钙储存位点中生理相关的钙通道或载体产生特异性作用来实现钙释放。InsP3引起的被动钙释放可被ATP和一种不可水解的ATP类似物5'-腺苷酰亚胺二磷酸增强，但不能被ADP或AMP增强。即使在0℃时也观察到了InsP3引起的被动钙释放。
