血管紧张素Ⅱ调节雄性大鼠催乳素和β-内啡肽的释放  

Effect of Angiotensin Ⅱ on prolactin and β-Endorphin Release in Male Rats

作　　者：韩小四[1] 许荣焜[1] 黄曼影[1] 单惠敏[1] 周远征[1] 郭传海[1] 黄醒亚[1] 

机构地区：[1]中国医学科学院基础医学研究所生理研究室,北京100005

出　　处：《基础医学与临床》1992年第6期40-45,共6页Basic and Clinical Medicine

基　　金：国家自然科学基金(编号38970313)

摘　　要：本工作给清醒、自由活动的SD雄性大鼠第三脑室内注射血管紧张素Ⅱ,用放射免疫测定给药前后血浆催乳素(PRL)和β-内啡肽(β-EP)含量的变化,结果显示,注射ANGⅡ50和500ng,可显著升高血浆PRL和β-EP的含量。静脉注射多巴胺受体阻断剂spiroperidol后,也可显著升高血浆PRL水平,若在此基础上加脑室内注射50ng ANGⅡ,血浆PRL含量与单独静脉注射spiroperidol无显著差别。在体外,ANGⅡ作用于前叶垂体细胞后,可使其培养液中PRL和β-EP含量显著升高。用EGTA络合细胞外Ca^(2+)后,不影响10^(-8)M ANGⅡ所致的PRL升高,但部分抑制其升高β-EP的效应。10^(-8)M的ANGⅡ可使垂体细胞内Ca^(2+)浓度显著升高,但不影响其胞内cAMP的含量。The present study was designed to examine the role of angiotensin Ⅱ (ANG Ⅱ) in the regulation of prolactin (PRL) and p-endorphin (β-EP) release and the mechanism of its action in vivo and in vitro. Injection of ANG Ⅰ into the third cerebroventricle (ICV) increased plasma PRL and β-EP. Iv injection of spiroperidol, a specific blocker of dopamine receptor, or iv injectio n of spiroperidol followed by ICV injection of ANG I (SOng/rat) increased plasma PRL, but had no significant change compared with each other. In vitro, ANG I caused does dependent release of PRL and β-EP from anterior pituitary cells. The depletion of external Ca2+ by EGTA partially supressed the ANG II induced PRL but not β-EP release. ANG Ⅱ caused increase of dispersed anterior pituitary cell cytoplasmic Ca2+ by 463%, but it did not change its cAMP content.

关 键 词：血管紧张素 催乳素 环磷酸腺苷 

分 类 号：R335.9[医药卫生—人体生理学]