Sobel D O
Peptides. 1984 Jan-Feb;5(1):47-51. doi: 10.1016/0196-9781(84)90049-4.
The effect of angiotensin II (Ang II) on pituitary beta endorphin like immunoactivity (beta END-LI) release was studied in monolayer culture of normal rat pituicites. Ang II stimulated beta END-LI release into the culture media. This release of beta END-LI increased with longer incubation time and with higher doses of Ang II. The beta END-LI response was similar to the pattern of Ang II mediated ACTH release. Ang II stimulated beta END-LI release was blocked by cycloheximide and decreased by corticosterone (5 nmol/l). Successively higher concentrations of [SAR GLY]Ang II, a known Ang II antagonist, induced greater inhibition of Ang II stimulated beta END-LI release. Gel chromatography of pooled media from control and Ang II stimulated cells revealed three peaks of beta END-LI which migrated with the void volume, beta lipotropin (beta LPH) and beta endorphin. The relative amount of beta END-LI in these peaks [(BEND-LI peak + total beta END-LI in column) x 100%] from media of control and stimulated cells were as follows: (1) Void 7% and 19% (2) beta LPH 50% and 52% (3) beta endorphin 43% and 29%.
在正常大鼠垂体细胞单层培养中研究了血管紧张素II（Ang II）对垂体β-内啡肽样免疫活性（β-END-LI）释放的影响。Ang II刺激β-END-LI释放到培养基中。β-END-LI的这种释放随着孵育时间延长和Ang II剂量增加而增加。β-END-LI反应与Ang II介导的促肾上腺皮质激素释放模式相似。Ang II刺激的β-END-LI释放被放线菌酮阻断，并被皮质酮（5 nmol/l）降低。已知的Ang II拮抗剂[SAR GLY]Ang II浓度依次升高，对Ang II刺激的β-END-LI释放的抑制作用增强。对来自对照细胞和Ang II刺激细胞的合并培养基进行凝胶过滤，显示出β-END-LI的三个峰，其与空体积、β-促脂素（β-LPH）和β-内啡肽一起迁移。对照细胞和刺激细胞培养基中这些峰中β-END-LI的相对含量[（β-END-LI峰+柱中总β-END-LI）×100%]如下：（1）空体积7%和19%；（2）β-LPH 50%和52%；（3）β-内啡肽43%和29%。
