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胰岛素对青蛙骨骼肌静息膜电位的作用机制。

Mechanism of insulin action on resting membrane potential of frog skeletal muscle.

作者信息

Moore R D, Rabovsky J L

出版信息

Am J Physiol. 1979 May;236(5):C249-54. doi: 10.1152/ajpcell.1979.236.5.C249.

DOI:10.1152/ajpcell.1979.236.5.C249
PMID:312605
Abstract

At a concentration that stimulates the Na pump, insulin hyperpolarizes the plasma membrane of frog sartorius in the presence of substrate-free Ringer. The hyperpolarization ranged from 3.5 to 7.3 mV and averaged 4.7 mV. Ouabain, 10(-4) M, completely blocked the effect of insulin on the membrane potential. Moreover, ouabain completely reversed the insulin-induced hyperpolarization within 20 min. The hyperpolarization produced by insulin was not associated with a detectable increase in the ratio of K+ permeability to Na+ permeability nor with a detectable increase in the concentration of intracellular K+, although a depletion of K+ near the external surface of the membrane cannot be excluded. The results clearly indicate that the hyperpolarization is secondary to stimulation of the Na pump by insulin.

摘要

在能刺激钠泵的浓度下,胰岛素在无底物任氏液存在时可使青蛙缝匠肌的质膜发生超极化。超极化幅度在3.5至7.3毫伏之间,平均为4.7毫伏。10⁻⁴ M的哇巴因完全阻断了胰岛素对膜电位的影响。此外,哇巴因在20分钟内完全逆转了胰岛素诱导的超极化。胰岛素产生的超极化与钾离子通透性与钠离子通透性的比值可检测到的增加无关,也与细胞内钾离子浓度可检测到的增加无关,尽管不能排除膜外表面附近钾离子的消耗。结果清楚地表明,超极化是胰岛素刺激钠泵的继发效应。

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Mechanism of insulin action on resting membrane potential of frog skeletal muscle.胰岛素对青蛙骨骼肌静息膜电位的作用机制。
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J Physiol. 1983 May;338:277-94. doi: 10.1113/jphysiol.1983.sp014673.
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Ouabain-resistant hyperpolarization induced by insulin in aggregates of embryonic heart cells.胰岛素在胚胎心脏细胞聚集体中诱导产生的哇巴因抗性超极化。
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