Weld M M, Fryer J N
Department of Anatomy, Faculty of Health Sciences, University of Ottawa, Canada.
Gen Comp Endocrinol. 1988 Mar;69(3):335-40. doi: 10.1016/0016-6480(88)90023-8.
The release of adrenocorticotropic hormone (ACTH) from dispersed goldfish anterior pituitary cells was examined in order to determine whether human angiotensin II (AII) would potentiate the ACTH-releasing activity of urotensin I (UI) and ovine corticotropin-releasing factor (oCRF), peptides with a sequence homology of greater than 50%. In mammals, AII has a slightly enhancing or potentiating effect on CRF-stimulated ACTH release. In the present investigations, concentrations of AII (0.5 and 1 nM), and of UI (1 nM) or oCRF (3 nM), which elicit moderate increases in ACTH release, were tested alone and in combination. The ACTH-releasing activities of AII and UI combined, or of AII and oCRF combined, showed no potentiation and in fact were less than additive. It was concluded that AII does not potentiate the ACTH-releasing activity of either UI or oCRF observed with goldfish anterior pituitary cells in vitro.
为了确定人血管紧张素II(AII)是否会增强尿紧张素I(UI)和羊促肾上腺皮质激素释放因子(oCRF)(序列同源性大于50%的肽)刺激金鱼垂体前叶细胞释放促肾上腺皮质激素(ACTH)的活性,对分散的金鱼垂体前叶细胞释放ACTH的情况进行了检测。在哺乳动物中,AII对CRF刺激的ACTH释放有轻微的增强或增效作用。在本研究中,单独及联合测试了能引起ACTH释放适度增加的AII(0.5和1 nM)、UI(1 nM)或oCRF(3 nM)的浓度。AII与UI联合或AII与oCRF联合刺激ACTH释放的活性并未增强,实际上还低于两者相加的效果。得出的结论是,在体外实验中,AII不会增强金鱼垂体前叶细胞中UI或oCRF刺激ACTH释放的活性。