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血管紧张素II对β-内啡肽样免疫反应性释放的体内和体外效应。

In vivo and in vitro effects of angiotensin II on the release of beta-endorphin-like immunoreactivity.

作者信息

Matsumura M, Inoue S, Yamanoi A, Chikamori K, Saito S

出版信息

Endocrinol Jpn. 1985 Apr;32(2):233-40. doi: 10.1507/endocrj1954.32.233.

Abstract

The effect of angiotensin II (A II) on the release of beta-endorphin-like immunoreactivity (beta-END-LI) in rats was studied in vivo and in vitro. Intravenous injection of 1 microgram/100 g body weight of A II resulted in significant increase in the plasma beta-END-LI level after 10 and 20 min. Intraventricular injection of 1 ng/100 g body weight of A II also resulted in significant increase in the plasma beta-END-LI level after 10 min. A II at concentrations of 10(-12) M-10(-10) caused dose-dependent stimulation of beta-END-LI release from dispersed cells of rat anterior pituitary. On gel chromatography, the beta-END-LI released by incubation of the cells with 10(-10) M A II separated into two components which eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. The ratio of beta-LPH to beta-END in these fractions was 5:1 on a molar basis. A II did not stimulate beta-END-LI release in Ca++-free-medium. [Sar1, Ala8]-A II at concentrations of 10(-9) M - 10(-7) M did not stimulate beta-END-LI release from the cells. Addition of [Sar1, Ala8]-A II to the incubation medium inhibited A II-induced beta-END-LI release from the cells. These results indicate that A II acts, at least in part, directly on anterior pituitary cells to stimulate beta-END-LI release and that calcium ion is involved in the mechanism of this effect.

摘要

在体内和体外研究了血管紧张素II(A II)对大鼠β-内啡肽样免疫反应性(β-END-LI)释放的影响。静脉注射1微克/100克体重的A II,10分钟和20分钟后血浆β-END-LI水平显著升高。脑室内注射1纳克/100克体重的A II,10分钟后血浆β-END-LI水平也显著升高。浓度为10(-12)M - 10(-10)的A II对大鼠垂体前叶分散细胞的β-END-LI释放具有剂量依赖性刺激作用。在凝胶色谱上,用10(-10)M A II孵育细胞释放的β-END-LI分离为两个组分,分别在与人β-促脂素和人β-内啡肽相同的位置洗脱。这些组分中β-LPH与β-END的摩尔比为5:1。A II在无Ca++培养基中不刺激β-END-LI释放。浓度为10(-9)M - 10(-7)M的[Sar1,Ala8]-A II不刺激细胞释放β-END-LI。向孵育培养基中添加[Sar1,Ala8]-A II可抑制A II诱导的细胞β-END-LI释放。这些结果表明,A II至少部分直接作用于垂体前叶细胞以刺激β-END-LI释放,并且钙离子参与了这种作用机制。

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