Gibson A, McFadzean I, Wallace P, Wayman C P
Biomedical Sciences Division, King's College London, UK.
Trends Pharmacol Sci. 1998 Jul;19(7):266-9. doi: 10.1016/s0165-6147(98)01222-x.
In many non-excitable cells, activation of phospholipase C-linked receptors results in a biphasic increase in the cytosolic Ca2+ concentration; an initial transient increase, owing to the release of Ca2+ from the endoplasmic/sarcoplasmic reticulum (ER/SR), is followed by a much smaller but sustained elevation, which often involves capacitative Ca2+ entry, where depletion of Ca2+ within the ER signals the opening of store-operated Ca2+ channels in the plasma membrane. However, in excitable cells such as smooth muscle, the role of capacitative Ca2+ entry is less clear and the main Ca2+ entry mechanisms responsible for sustained cellular activation have been considered to be either voltage-operated or receptor-operated Ca2+ channels. Although store-regulated Ca2+ entry was known to occur following agonist activation of smooth muscle, it was believed to be important only for the re-filling of the depleted SR and not as a source of activator Ca2+ for the contractile mechanisms. Here, Alan Gibson, Ian McFadzean, Pat Wallace and Christopher Wayman review recent evidence that capacitative Ca2+ entry might indeed be important for the regulation of smooth muscle tone, and that it might provide an important for pharmacological intervention.
在许多非兴奋性细胞中，磷脂酶C偶联受体的激活会导致胞质Ca2+浓度出现双相增加；最初的短暂增加是由于内质网/肌浆网（ER/SR）释放Ca2+，随后是幅度小得多但持续的升高，这通常涉及容量性Ca2+内流，即ER内Ca2+的耗竭会引发质膜中储存操纵性Ca2+通道的开放。然而，在平滑肌等可兴奋细胞中，容量性Ca2+内流的作用尚不清楚，而负责细胞持续激活的主要Ca2+内流机制被认为是电压门控或受体门控Ca2+通道。尽管已知激动剂激活平滑肌后会发生储存调节性Ca2+内流，但人们认为它仅对耗尽的SR的重新填充很重要，而不是作为收缩机制中激活Ca2+的来源。在此，艾伦·吉布森、伊恩·麦克法泽恩、帕特·华莱士和克里斯托弗·韦曼综述了近期的证据，即容量性Ca2+内流可能确实对平滑肌张力的调节很重要，并且它可能为药物干预提供重要途径。
