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SF Kan1 , MM Kau1 , SC Tsai1 *, JJ Chen1 *, PS Wang1 *
Dept. Physiol., Nalt. Yang-Ming Univ., Taipei, Taiwan, ROC 1
It has been known that hyperprolactinemia activates the hypothalamic-pituitary-adrenal axis. However, the role of prolactin (PRL) in regulating glucocorticoid secretion is not very clear. The present study was to investigate the effects of bromocriptine-induced hypoprolactinemia on corticosterone production in rats. Male rats were treated with or without bromocriptine (5 mg/kg, s.c.) twice per day for 2 days before decapitation. The adrenal zona fasciculata-reticularis (ZFR) cells were prepared and incubated with adrenocorticotropic hormone (ACTH), forskolin (an adenylyl cyclase activator), 8-bromo-adenosine 3': 5' cyclic monophosphate (8-Br-cAMP, a membrane-permeable analog of cAMP) and steroidogenic precursors including 25-OH-cholesterol, pregnenolone, progesterone and deoxycorticosterone. Administration of bromocriptine in vivo resulted in a decrease in the levels of plasma PRL and corticosterone. Both basal and ACTH-stimulated corticosterone secretions by ZFR cells were also lower in hypoprolactinemic rats than in control animals. Likewise, the corticosterone production induced by forskolin was lower in hypoprolactinemic rats than in control animals. After incubation of 8-Br-cAMP, there was no difference in the release of corticosterone between control and hypoprolactinemic groups. Incubation of ZFR cells with steroidogenic precursors, only the corticosterone release induced by 25-OH-cholesterol was lower in hypoprolactinemic than in control group. Administration of bromocriptine in vitro did not alter the release of corticosterone by rat ZFR cells. These results suggest that bromocriptine-induced hypoprolactinemia decreases the steroidogensis of corticosterone through inhibition of the activities of adenylyl cyclase and desmolase (P450scc) in ZFR cells.
This abstract is being presented on Sunday, August 1 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.