Flatman J A, Clausen T
Nature. 1979 Oct 18;281(5732):580-1. doi: 10.1038/281580a0.
Both beta 2-adrenoreceptor stimulants (such as adrenaline and salbutamol) and insulin can increase active Na+-K+ transport and hyperpolarise skeletal cells. Thus, adrenaline and insulin, which are otherwise antagonistic regulators of several metabolic processes, have one action in common, namely, stimulation of active ion translocation. This is especially interesting as cyclic AMP stimulates Na+-K+ transport, whereas a lowering of the cytoplasmic concentration of cyclic AMP has been proposed as an early signal in the action of insulin. Here we report the results of experiments in which the active Na+-K+ transport and membrane potential (EM) of rat soleus muscles were studied during the action of supramaximal doses of insulin and beta 2-adrenoreceptor stimulants, alone and in combination. We conclude that the stimulant action of insulin on active electrogenic Na+-K+ transport is unlikely to be evoked by a lowering of the intracellular concentration of cyclic AMP.
β2-肾上腺素能受体激动剂(如肾上腺素和沙丁胺醇)以及胰岛素均可增强活性Na+-K+转运,并使骨骼肌细胞超极化。因此,肾上腺素和胰岛素虽在其他几个代谢过程中是拮抗调节因子,但它们有一个共同作用,即刺激活性离子转运。这一点尤为有趣,因为环磷酸腺苷(cAMP)可刺激Na+-K+转运,而细胞内cAMP浓度降低被认为是胰岛素作用的早期信号。在此,我们报告了相关实验结果,该实验研究了超最大剂量胰岛素和β2-肾上腺素能受体激动剂单独及联合作用时大鼠比目鱼肌的活性Na+-K+转运和膜电位(EM)。我们得出结论,胰岛素对活性生电Na+-K+转运的刺激作用不太可能由细胞内环磷酸腺苷浓度降低引起。