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关于儿茶酚胺诱导骨骼肌细胞超极化的机制

On the mechanism of catecholamine-induced hyperpolarization of skeletal muscle cells.

作者信息

Zemková H, Svoboda P, Teisinger J, Vyskocil F

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1985 Mar;329(1):18-23. doi: 10.1007/BF00695186.

Abstract

Catecholamines (noradrenaline, adrenaline and isoprenaline) were tested for their effect on the resting membrane potential of mouse skeletal muscle cells. In freshly isolated muscles incubated in the normal solution containing 5 mol . l-1, catecholamines increased the resting membrane potential (RMP) by 3-5 mV. In Na+-loaded muscles incubated in a K+-free solution, however, catecholamines increased the RMP by 13-16 mV; consequent application of K+ to these muscles did not hyperpolarize the membrane further. A significant decrease of input membrane resistance was observed during the noradrenaline-induced hyperpolarization. This indicates that the passive membrane permeability for K+ ions was apparently increased. Noradrenaline-induced hyperpolarization requires the presence of calcium ions in the incubation solution. We therefore assume that catecholamines hyperpolarize the membrane by Ca2+-dependent K+-channels activation. The action of catecholamines on the resting membrane potential of skeletal muscle exhibits a 50% nonspecific effect as far as the adrenergic receptor is concerned, and the rest may be blocked by adrenergic blocking agents.

摘要

研究了儿茶酚胺(去甲肾上腺素、肾上腺素和异丙肾上腺素)对小鼠骨骼肌细胞静息膜电位的影响。在含有5 mol·l⁻¹的正常溶液中孵育的新鲜分离肌肉中,儿茶酚胺使静息膜电位(RMP)升高3 - 5 mV。然而,在无钾溶液中孵育的钠负载肌肉中,儿茶酚胺使RMP升高13 - 16 mV;随后向这些肌肉施加钾离子并未使膜进一步超极化。在去甲肾上腺素诱导的超极化过程中,观察到输入膜电阻显著降低。这表明钾离子的被动膜通透性明显增加。去甲肾上腺素诱导的超极化需要孵育溶液中存在钙离子。因此,我们推测儿茶酚胺通过依赖钙离子的钾通道激活使膜超极化。就肾上腺素能受体而言,儿茶酚胺对骨骼肌静息膜电位的作用有50%是非特异性的,其余部分可能被肾上腺素能阻断剂阻断。

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