Wang X, Chik C L, Ho A K, Sato N, Greer M A
Department of Medicine, Oregon Health Sciences University, Portland 97201.
Metabolism. 1993 Apr;42(4):435-9. doi: 10.1016/0026-0495(93)90099-a.
We have evaluated whether cyclic adenosine monophosphate (cAMP) generation plays a role in the burst of hormone secretion caused by osmotic cell-swelling in tumor-derived and normal pituitary cells. Up to 45% hyposmolarity induced a dose-dependent increase in prolactin (PRL) secretion, but had no effect on cAMP generation. However, hyposmolarity inhibited forskolin-induced cAMP accumulation in a dose-dependent manner, but had no effect on 3-isobutyl-1-methyl-xanthine (IBMX)-induced cAMP accumulation. Ca2+ depletion of the medium partially blocked the inhibitory effect of hyposmolarity on forskolin-induced cAMP generation and completely blocked stimulation of PRL secretion by hyposmolarity. High levels of K+ in medium inhibited forskolin-induced cAMP generation, while thyrotropin-releasing hormone (TRH) enhanced it. Our results indicate that in both GH4C1 and normal pituitary cells, cAMP is not a regulatory factor for hormone secretion induced by cell-swelling.
我们评估了环磷酸腺苷（cAMP）生成在肿瘤来源的垂体细胞和正常垂体细胞中因渗透性细胞肿胀引起的激素分泌爆发中是否起作用。高达45%的低渗状态诱导催乳素（PRL）分泌呈剂量依赖性增加，但对cAMP生成没有影响。然而，低渗状态以剂量依赖性方式抑制福司可林诱导的cAMP积累，但对3 - 异丁基 - 1 - 甲基黄嘌呤（IBMX）诱导的cAMP积累没有影响。培养基中Ca2+耗竭部分阻断了低渗状态对福司可林诱导的cAMP生成的抑制作用，并完全阻断了低渗状态对PRL分泌的刺激作用。培养基中高浓度的K+抑制福司可林诱导的cAMP生成，而促甲状腺激素释放激素（TRH）则增强其生成。我们的结果表明，在GH4C1细胞和正常垂体细胞中，cAMP都不是细胞肿胀诱导的激素分泌的调节因子。
