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[缓激肽对β-内啡肽样免疫反应性释放的体内和体外作用]

[In vivo and in vitro effects of bradykinin on the release of beta-endorphin-like immunoreactivity].

作者信息

Shimizu I, Matsumura M

出版信息

Nihon Naibunpi Gakkai Zasshi. 1985 Dec 20;61(12):1330-40. doi: 10.1507/endocrine1927.61.12_1330.

Abstract

The effect of bradykinin (BK) on the release of beta-endorphin-like immunoreactivity (beta-END-LI) in rats was studied in in vivo and in vitro. Intraperitoneal injection of BK at 5 micrograms/100 g body weight resulted in a significant increase in the plasma beta-END-LI level after 15 min. BK at concentrations of 10(-12)-10(-7) M also caused dose-dependent stimulation of beta-END-LI release from the dispersed cells of the anterior pituitary of rats. On gel chromatography, the beta-END-LI released by incubation of the cells with 10(-7) M BK separated into two components; one eluted in the same positions as human beta-lipotropin and the other as human beta-endorphin. BK did not stimulate beta-END-LI release in Ca++-free medium. Addition of 10(-3) M verapamil, 10(-6) M dexamethasone or 10(-7) M somatostatin to the incubation medium inhibited BK-induced beta-END-LI release from the cells. Ouabain (10(-5) M) also stimulated beta-END-LI release, but its effect was not additive with that of BK. These results indicate that BK stimulates beta-END-LI release and that calcium ion is involved in the mechanism of this effect.

摘要

研究了缓激肽(BK)对大鼠体内和体外β-内啡肽样免疫反应性(β-END-LI)释放的影响。以5微克/100克体重腹腔注射BK,15分钟后血浆β-END-LI水平显著升高。浓度为10^(-12)-10^(-7)M的BK也能剂量依赖性地刺激大鼠垂体前叶分散细胞释放β-END-LI。在凝胶色谱分析中,细胞与10^(-7)M BK孵育释放的β-END-LI分离为两个组分;一个与人类β-促脂素在相同位置洗脱,另一个与人类β-内啡肽在相同位置洗脱。BK在无Ca++的培养基中不刺激β-END-LI释放。向孵育培养基中添加10^(-3)M维拉帕米、10^(-6)M地塞米松或10^(-7)M生长抑素可抑制BK诱导的细胞β-END-LI释放。哇巴因(10^(-5)M)也刺激β-END-LI释放,但其作用与BK的作用无相加性。这些结果表明BK刺激β-END-LI释放,且钙离子参与了这一效应的机制。

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