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肾上腺素对大鼠胰岛胰岛素释放及⁸⁶Rb⁺或⁴⁵Ca²⁺通量的影响。

Epinephrine modifications of insulin release and of 86Rb+ or 45Ca2+ fluxes in rat islets.

作者信息

Tamagawa T, Henquin J C

出版信息

Am J Physiol. 1983 Mar;244(3):E245-52. doi: 10.1152/ajpendo.1983.244.3.E245.

DOI:10.1152/ajpendo.1983.244.3.E245
PMID:6338738
Abstract

The effects of epinephrine on insulin release, 86Rb+ fluxes, and 45Ca2+ fluxes were measured in rat islets. In the presence of 10 mM glucose, epinephrine did not affect 86Rb+ influx and slightly increased net uptake. It caused a monophasic inhibition of release and a biphasic decrease in 86Rb+ efflux. A maximum effect was observed with 1 microM epinephrine, but release was more markedly inhibited by lower concentrations of the catecholamine than was the efflux. Epinephrine inhibition of release and efflux was reversed by phentolamine and yohimbine but not by prazosin or propranolol. It was mimicked by norepinephrine and clonidine. The inhibition of 86Rb+ efflux persisted when insulin release was prevented by omission of extracellular calcium. Ouabain or high K+ markedly increased 86Rb+ efflux in the presence of glucose and epinephrine; theophylline and quinine had a similar but smaller effect. None of these agents restored insulin release. Epinephrine abolished the insulinotropic effect of arginine without altering the rise in 86Rb+ efflux triggered by the amino acid. Epinephrine abolished insulin release but inhibited 45Ca2+ efflux only partially during stimulation by glucose or by barium plus theophylline. The results show that epinephrine does not inhibit insulin release by activating the Na pump or by increasing K permeability of the B cell membrane. On the contrary, the inhibition of release is accompanied by a decrease in 86Rb+ efflux. Both result from activation of alpha 2-receptors but are not causally related; they could be due to remodeling of Ca2+ fluxes and/or changes in cAMP levels.

摘要

在大鼠胰岛中测量了肾上腺素对胰岛素释放、⁸⁶Rb⁺通量和⁴⁵Ca²⁺通量的影响。在10 mM葡萄糖存在的情况下,肾上腺素不影响⁸⁶Rb⁺内流,且略微增加净摄取量。它引起释放的单相抑制和⁸⁶Rb⁺外流的双相减少。在1 μM肾上腺素时观察到最大效应,但较低浓度的儿茶酚胺对释放的抑制作用比对外流的抑制作用更明显。肾上腺素对释放和外流的抑制作用可被酚妥拉明和育亨宾逆转,但不能被哌唑嗪或普萘洛尔逆转。去甲肾上腺素和可乐定可模拟这种作用。当通过省略细胞外钙来阻止胰岛素释放时,⁸⁶Rb⁺外流的抑制作用仍然存在。哇巴因或高钾在葡萄糖和肾上腺素存在的情况下显著增加⁸⁶Rb⁺外流;茶碱和奎宁有类似但较小的作用。这些药物均未恢复胰岛素释放。肾上腺素消除了精氨酸的促胰岛素作用,但未改变氨基酸引发的⁸⁶Rb⁺外流增加。肾上腺素消除了胰岛素释放,但在葡萄糖或钡加茶碱刺激期间仅部分抑制⁴⁵Ca²⁺外流。结果表明,肾上腺素不是通过激活钠泵或增加B细胞膜的钾通透性来抑制胰岛素释放。相反,释放的抑制伴随着⁸⁶Rb⁺外流的减少。两者均源于α₂受体的激活,但并非因果相关;它们可能是由于Ca²⁺通量的重塑和/或cAMP水平的变化。

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