Jenkinson D H, Haylett D G, Cook N S
Cell Calcium. 1983 Dec;4(5-6):429-37. doi: 10.1016/0143-4160(83)90019-2.
Activation of certain membrane receptors increases the concentration of Ca2+ in the cytosol of hepatocytes. Since in most species these cells possess a PK(Ca) mechanism, the outcome is a rise in PK. This can be blocked by quinine, apamin and certain neuromuscular blocking agents. The binding of labelled apamin to hepatocytes has been studied under physiological conditions, and the relationship between the binding sites and K+ channels is discussed. The physiological role of the PK(Ca) mechanism in hepatocytes is unclear, though it is largely responsible for 'adrenaline hyperkalaemia'.
某些膜受体的激活会增加肝细胞胞质溶胶中Ca2+的浓度。由于在大多数物种中,这些细胞具有蛋白激酶C(钙依赖)(PK(Ca))机制,其结果是蛋白激酶C(PK)水平升高。这可被奎宁、蜂毒明肽和某些神经肌肉阻滞剂阻断。已在生理条件下研究了标记的蜂毒明肽与肝细胞的结合,并讨论了结合位点与钾通道之间的关系。肝细胞中PK(Ca)机制的生理作用尚不清楚,尽管它在很大程度上导致了“肾上腺素高钾血症”。