Matsumura M, Ohura M, Shimizu I, Yamonoi A, Iwasaki A, Saito S
Neuroendocrinology. 1985 Aug;41(2):101-6. doi: 10.1159/000124161.
The effect of bradykinin (BK) on the release of beta-endorphin-like immunoreactivity (beta-EpLI) in rats was studied in vivo and in vitro. Intraperitoneal injection of BK at 5 micrograms/100 g body weight resulted in significant increase in the plasma beta-EpLI level after 15 min. BK at concentrations of 10(-12)-10(-7) M also caused dose-dependent stimulation of beta-EpLI release from dispersed cells of rat anterior pituitary. On gel chromatography, the beta-EpLI released by incubation of the cells with 10(-7) M BK separated into two components, eluted in the same positions as human beta-lipotropin and human beta-endorphin, respectively. BK did not stimulate beta-EpLI release in Ca++-free medium. Addition of 10(-3) M verapamil or 10(-6) M dexamethasone to the incubation medium inhibited BK-induced beta-EpLI release from the cells. Quabain (10(-5) M) also stimulated beta-EpLI release, but its effect was not additive with that of BK. These results indicate that BK stimulates beta-EpLI release and that calcium ion is involved in the mechanism of this effect.
在体内和体外研究了缓激肽(BK)对大鼠β-内啡肽样免疫反应性(β-EpLI)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-EpLI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-EpLI。在凝胶色谱上,细胞与10^(-7) M BK孵育释放的β-EpLI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。BK在无钙培养基中不刺激β-EpLI释放。向孵育培养基中加入10^(-3) M维拉帕米或10^(-6) M地塞米松可抑制BK诱导的细胞β-EpLI释放。哇巴因(10^(-5) M)也刺激β-EpLI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-EpLI释放,且钙离子参与了这一效应的机制。