Inoue S, Matsumura M
Nihon Naibunpi Gakkai Zasshi. 1986 Mar 20;62(3):158-68. doi: 10.1507/endocrine1927.62.3_158.
The effect of histamine on the release of beta-endorphin-like immunoreactivity (beta-END LI) in rats was studied in vivo and in vitro experiments. Intravenous injection of 100 micrograms/100g BW of histamine resulted in a significant increase in the plasma beta-END-LI level 5, 15 minutes after the injection. Histamine at concentrations of 10(-12) to 10(-9)M also caused dose-dependent stimulation of release of beta-END-LI from the dispersed cells of the anterior pituitary of rats. On gel-chromatography, the beta-END-LI released by incubating the cells with 10(-9)M histamine consisted of two components, which eluted in the same positions as human beta-lipotropin and human endorphin, respectively. Addition of 2mM CoCl2 to the incubation medium inhibited histamine-induced beta-END LI release from the cells. Histamine H1 receptor antagonist (10(-6)M) inhibited histamine-induced beta-END-LI release from the cells. Histamine H2 receptor antagonist (10(-6)M), however, did not inhibit histamine-induced beta-END-LI release. These results indicate that histamine acts directly on the anterior pituitary cells to stimulate beta-END-LI release and that calcium ion is involved in the mechanism of this effect.
通过体内和体外实验研究了组胺对大鼠β-内啡肽样免疫反应性(β-END LI)释放的影响。静脉注射100微克/100克体重的组胺后,注射后5分钟和15分钟血浆β-END-LI水平显著升高。浓度为10(-12)至10(-9)M的组胺也引起大鼠垂体前叶分散细胞β-END-LI释放的剂量依赖性刺激。在凝胶色谱上,用10(-9)M组胺孵育细胞释放的β-END-LI由两个组分组成,它们分别在与人β-促脂素和人内啡肽相同的位置洗脱。向孵育培养基中加入2mM CoCl2可抑制组胺诱导的细胞β-END LI释放。组胺H1受体拮抗剂(10(-6)M)抑制组胺诱导的细胞β-END-LI释放。然而,组胺H2受体拮抗剂(10(-6)M)不抑制组胺诱导的β-END-LI释放。这些结果表明,组胺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的机制。