Reyl-Desmars F, Zeytin F
Biochem Biophys Res Commun. 1985 Mar 29;127(3):986-91. doi: 10.1016/s0006-291x(85)80041-3.
GH3 cells were used to study the effect of rat growth hormone-releasing factor on adenylate cyclase activity and its interaction with somatostatin. Rat GRF stimulates adenylate cyclase activity (ED5 0 = 6 X 10(-8) M) and somatostatin-14 inhibits this GRF-stimulated activity in a non-competitive manner without affecting the basal enzyme levels. Inhibition by somatostatin-14 is observed at concentrations as low as 10(-11) M and the half-maximal effect is obtained with 10(-8) M. Somatostatin-28 is more potent than SS-14 and has an ED5 0 of 3 X 10(-11) M. VIP is more active than rat GRF in stimulating adenylate cyclase activation. We conclude that in GH3 cells rat GRF behaves as a partial VIP agonist by interacting with VIP-preferring receptors and its effects are inhibited by somatostatin.
利用GH3细胞研究大鼠生长激素释放因子对腺苷酸环化酶活性的影响及其与生长抑素的相互作用。大鼠生长激素释放因子刺激腺苷酸环化酶活性（半数有效剂量=6×10⁻⁸ M），生长抑素-14以非竞争性方式抑制这种生长激素释放因子刺激的活性，且不影响基础酶水平。在低至10⁻¹¹ M的浓度下即可观察到生长抑素-14的抑制作用，半数最大效应在10⁻⁸ M时获得。生长抑素-28比生长抑素-14更有效，半数有效剂量为3×10⁻¹¹ M。血管活性肠肽在刺激腺苷酸环化酶激活方面比大鼠生长激素释放因子更具活性。我们得出结论，在GH3细胞中，大鼠生长激素释放因子通过与偏好血管活性肠肽的受体相互作用，表现为部分血管活性肠肽激动剂，其作用受到生长抑素的抑制。
