钙拮抗剂尼莫地平通过作用于肾上腺增加大鼠垂体β-内啡肽的释放。一项“体内”和“体外”研究。

The calcium antagonist nimodipine increases beta-endorphin release from rat hypophysis through an action on adrenal glands. An "in vivo" and "in vitro" study.

作者信息

Costa G, Saija A, Padovano I, Trimarchi G R, De Pasquale R, Caputi A P

出版信息

Pharmacol Res Commun. 1984 Oct;16(10):959-68. doi: 10.1016/s0031-6989(84)80060-0.

Abstract

Intravenous injection of nimodipine (1, 10 and 100 micrograms/Kg) raised plasma ACTH and beta-endorphin (beta-EP) level and reduced pituitary beta-EP content, in the rat. These effects were sharp and short-lasting. Nimodipine (10(-8), 10(-7), 10(-6) M) did not change basal and hypothalamic extract stimulated beta-EP release from pituitary tissue in vitro. Basal release of corticosterone from adrenal glands, superfused in vitro with the calcium antagonist (10(-7) - 10(-6) M), was not modified. However, ACTH-induced release was strongly reduced. Since glucocorticoids feedback regulates biosynthesis and cleavage of pro-opiocortin, nimodipine, which reduces adrenal gland responsiveness to ACTH, might reflexly increase beta-EP release from hypophysis.

摘要

静脉注射尼莫地平（1、10和100微克/千克）可提高大鼠血浆促肾上腺皮质激素（ACTH）和β-内啡肽（β-EP）水平，并降低垂体β-EP含量。这些作用迅速且持续时间短。尼莫地平（10^(-8)、10^(-7)、10^(-6) M）在体外并未改变基础状态下以及下丘脑提取物刺激垂体组织释放β-EP的情况。体外与钙拮抗剂（10^(-7) - 10^(-6) M）共同孵育时，肾上腺皮质酮的基础释放未受影响。然而，ACTH诱导的释放则显著减少。由于糖皮质激素通过反馈调节促阿片-促皮质素原的生物合成和裂解，尼莫地平降低了肾上腺对ACTH的反应性，可能会反射性地增加垂体β-EP的释放。