Direct effects of prolactin an corticosterone release by zona fasciculata-reticularis cells from male rats

The role of prolactin (PRL) in the male is not fully defined. The aim of th is study was to investigate the function and mechanism of PRL on the produc tion of corticosterone by zona fasciculata-reticularis (ZFR) cells in vitro . The ZFR cells were obtained from male rats under normal, hyperprolactinem ic, or hypoprolactinemic situation. PRL stimulated the corticosterone relea se in a dose-dependent pattern in the ZFR cells from normal male rats. The cellular adenosine 3'-5'-cyclic monophosphate (cAMP) concentration positive ly correlated with PRL concentration in the presence of forskolin or 3-isob utyl-1-methylxanthine (IBMX). PRL enhanced the stimulatory effects of cAMP mimetic reagents, i.e., forskolin, 8-bromo-adenosine 3',5'-cyclic monophosp hate (8-Br-cAMP), and IBMX on the release of corticosterone. The adenylate cyclase inhibitor (SQ22536) inhibited the corticosterone release in spite o f presence of PRL. Nifedipine (L-type calcium channel blocker) did not inhi bit corticosterone release. The hyperprolactinemic condition was actualized by transplantation of donor rat anterior pituitary glands (APs) under kidn ey capsule. By comparison with the cerebral cortex (CX)-grafted group, AP-g raft resulted in an increased release of corticosterone, 3 beta-hydroxyster iod dehydrogenase (HSD) activity and cAMP production by ZFR cells. Acute hy poprolactinemic status was induced by bromocriptine for 2 days. The results showed the productions of corticosterone were lower in hypoprolactinemic g roup than in control group, which were persistent along with different ACTH concentrations. These results suggest that PRL increase the release of cor ticosterone by ZFR cells via cAMP cascades and 3 beta-HSD activity. (C) 199 9 Wiley-Liss, Inc.