Ruiz-Ceretti E, DeLorenzi F, Lafond J S, Chartier D
Department of Physiology and Biophysics, Faculty of Medicine, University of Sherbrooke, Qué., Canada.
Can J Physiol Pharmacol. 1988 Mar;66(3):202-6. doi: 10.1139/y88-035.
Insulin stimulates ionic transport by the sodium pump and induces hyperpolarization in skeletal and cardiac muscle among other cells. The insulin-induced hyperpolarization in most cases can be inhibited by exposure to cardiac glycosides or metabolic inhibition. However, extracellular accumulation of K ions leaking from hypoxic cells in superfused preparations may distort the effects of insulin on the resting potential. We used standard microelectrode techniques and perfused rabbit hearts submitted to hypoxia and substrate deprivation to reinvestigate the effects of insulin (6.4 nM) on the membrane potential. The membrane depolarized by about 6 mV and the action potential was reduced to a sharp spike without overshoot. Insulin restored the resting potential to control values but did not change the action potential configuration substantially. The insulin-induced repolarization was not due to reuptake of potassium as revealed by spectrophotometric determinations of myocardial K content. In addition, the diffusion component of the resting potential measured after inhibition of the sodium pump with 10(-4) M ouabain was not modified by insulin. Our results suggest that an increase in the contribution of electrogenic Na extrusion to the resting potential underlies the repolarizing effect of insulin of hypoxic substrate-deprived myocardium.
胰岛素通过钠泵刺激离子转运，并在骨骼肌、心肌等多种细胞中诱导超极化。在大多数情况下，胰岛素诱导的超极化可被暴露于强心苷或代谢抑制所抑制。然而，在灌注制备物中，缺氧细胞泄漏的钾离子在细胞外的积累可能会扭曲胰岛素对静息电位的影响。我们使用标准微电极技术，对处于缺氧和底物剥夺状态的兔心脏进行灌注，以重新研究胰岛素（6.4 nM）对膜电位的影响。膜电位去极化约6 mV，动作电位降至尖锐的峰电位且无超射。胰岛素将静息电位恢复到对照值，但对动作电位的形态没有实质性改变。分光光度法测定心肌钾含量显示，胰岛素诱导的复极化并非由于钾的再摄取。此外，用10⁻⁴ M哇巴因抑制钠泵后测得的静息电位的扩散成分不受胰岛素影响。我们的结果表明，在缺氧底物剥夺的心肌中，电生性钠外流对静息电位的贡献增加是胰岛素复极化作用的基础。
