Cyclic adenosine monophosphate is not part of the transduction chain by which cell-swelling induces secretion in either normal or tumor-derived GH4C1 pituitary cells.

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.