Nakipova O V, Kokoz Iu M, Lazarev A V, Freĭdin A A, Krupenin V A
Fiziol Zh SSSR Im I M Sechenova. 1988 Mar;74(3):420-7.
The inhibitory effect of insulin on Ca2+-current was supposed to be due to activation of phosphoproteinphosphotases stimulated by a specific intracellular insulin messenger. The results obtained support the above suggestion. Pretreatment of myocardial preparation with cycloheximide in low concentrations completely blocks the inhibitory insulin effect on Ca2+-current due, probably, to a decrease in peptide formation. Moreover, prolonged effect of the hormone involves a considerable increase of the current as compared to its initial value. Possible mechanisms of modifying effect of cycloheximide on the function of insulin-dependent regulatory system in the myocardium, are discussed.
胰岛素对钙离子电流的抑制作用被认为是由于一种特定的细胞内胰岛素信使刺激了磷酸蛋白磷酸酶的激活。所获得的结果支持上述观点。用低浓度的环己酰亚胺预处理心肌制剂，可能由于肽形成的减少，完全阻断了胰岛素对钙离子电流的抑制作用。此外，与初始值相比，激素的长期作用会使电流显著增加。本文讨论了环己酰亚胺对心肌中胰岛素依赖性调节系统功能的修饰作用的可能机制。
