Sheppard M S, Moor B C, Kraicer J
Endocrinology. 1985 Dec;117(6):2364-70. doi: 10.1210/endo-117-6-2364.
An acutely dispersed and purified preparation of somatotrophs obtained from rat adenohypophyses was used to study the mechanism of action of GH-releasing factor (GRF). Synthetic GRF [human pancreatic, hpGRF-(1-40)-OH] stimulated the immediate (within 4 min) release of GH in a dose-related manner, with a preceding or concurrent increase in cAMP in the somatotrophs. Somatostatin, at concentrations as low as 1.0 ng/ml, completely blocked the GRF-induced increase in GH release, with only a partial reduction in the GRF-induced accumulation of cAMP in the somatotrophs. 3-Isobutyl-1-methylxanthine, a phosphodiesterase inhibitor, potentiated the action of GRF in increasing cAMP in the somatotrophs, with subsequent GH release. These results along with those of previous studies suggest that cAMP is an intracellular mediator in the action of GRF and that somatostatin has a major effect on blocking GH release at a step subsequent to cAMP accumulation.
从大鼠腺垂体获得的急性分散和纯化的生长激素细胞制剂用于研究生长激素释放因子(GRF)的作用机制。合成的GRF [人胰腺,hpGRF-(1-40)-OH] 以剂量相关的方式刺激生长激素的即时(4分钟内)释放,同时生长激素细胞中的cAMP会提前或同时增加。生长抑素,低至1.0 ng/ml的浓度,完全阻断了GRF诱导的生长激素释放增加,而在生长激素细胞中GRF诱导的cAMP积累仅部分减少。磷酸二酯酶抑制剂3-异丁基-1-甲基黄嘌呤增强了GRF在增加生长激素细胞中cAMP方面的作用,并随后释放生长激素。这些结果以及先前研究的结果表明,cAMP是GRF作用中的细胞内介质,并且生长抑素在cAMP积累后的步骤中对阻断生长激素释放具有主要作用。