| Abstract: | The ovary and adenohypophysis of the rat contain beta-adrenergic receptors and respond to beta-adrenergic stimulation with hormone release. To determine the importance of the adrenal medulla as a source of adrenergic influences regulating prepubertal ovarian and pituitary function, a technique was developed to remove most of the adrenal medulla without compromising adrenocortical function. Medullectomy (MED) of 24-day-old female rats depressed both spontaneous diurnal changes in plasma epinephrine (EPI), and the EPI and norepinephrine (NE) response to decapitation, without affecting corticosterone (B) levels. Vaginal opening and first ovulation were delayed in MED rats. Serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels were normal in MED rats, but those of growth hormone (GH) and prolactin (Prl) were depressed. MED reduced the ovarian weight response to pregnant mare's serum gonadotropin (PMSG) and the ovarian steroidal response to human chorionic gonadotropin (hCG) in vitro, but it did not affect ovarian beta-adrenergic receptors. Cultured granulosa cells, harvested from juvenile ovaries and primed in vitro with FSH, responded to nanomolar concentrations of EPI with progesterone (P) secretion. EPI also augmented hCG- and FSH-induced P secretion. The EPI effect was reproduced by Zinterol, a beta 2-adrenergic agonist and was prevented by propranolol, a beta-adrenergic antagonist. Blockade of alpha-adrenergic receptors with phentolamine was ineffective. It is suggested that EPI of adrenomedullary origin supports female prepubertal development by a) stimulating ovarian P secretion, b) favoring Prl and GH release and c) amplifying the stimulatory effect of low gonadotropin levels on ovarian steroidogenesis. The effects of EPI on ovarian function appear to be mediated by beta-adrenergic receptors of the beta 2 type. |
