Takemura H, Ohshika H
Department of Pharmacology, Sapporo Medical College, Japan.
Nihon Yakurigaku Zasshi. 1991 Jun;97(6):319-27. doi: 10.1254/fpj.97.6_319.
Inositol phosphates have an important role in Ca2+ mobilization and especially inositol 1, 4, 5-trisphosphate (IP3) is now believed to release Ca2+ from the endoplasmic reticulum (ER). On the other hand, the mechanism of activation of Ca2+ entry is unknown. Non-excitable cells have only receptor-operated Ca2+ channels, lacking voltage-operated Ca2+ channels, and are a useful system for studying signal transduction. In this review, some mechanisms for the regulation of Ca2+ entry in non-excitable cells are discussed and a new hypothesis originally proposed by Putney (1986), the capacitative Ca2+ entry model, is focussed. In this model, Ca2+ influx across the plasma membrane is increased when the IP3-sensitive Ca2+ pools is emptied. Capacitative Ca2+ entry is now confirmed in rat parotid acinar cells by studies on the refilling process for intracellular Ca2+ pools and by using the microsomal Ca(2+)-ATPase inhibitor thapsigargin, which does not increase cellular IP3. Finally, capacitative Ca2+ entry is expected to exist in a variety of cell types including excitable cells.
肌醇磷酸在钙离子动员中起着重要作用，尤其是现在认为肌醇1,4,5 - 三磷酸（IP3）能从内质网（ER）释放钙离子。另一方面，钙离子内流的激活机制尚不清楚。非兴奋性细胞仅具有受体操纵的钙离子通道，缺乏电压操纵的钙离子通道，是研究信号转导的有用系统。在这篇综述中，讨论了非兴奋性细胞中钙离子内流的一些调节机制，并重点介绍了Putney（1986年）最初提出的一个新假说——容量性钙离子内流模型。在这个模型中，当IP3敏感的钙离子池排空时，跨质膜的钙离子内流增加。现在通过对细胞内钙离子池再填充过程的研究以及使用不增加细胞IP3的微粒体钙（2 +）-ATP酶抑制剂毒胡萝卜素，在大鼠腮腺腺泡细胞中证实了容量性钙离子内流。最后，预计容量性钙离子内流存在于包括兴奋性细胞在内的多种细胞类型中。
