Mifepristone treatment demonstrates the participation of adrenal glucocorticoids in the regulation of oestrogen-induced prolactin secretion in ovariectomized rats.

CARÓN, R.W.; SALICIONI, A.M.; DEIS, R.P.

JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY

Año: 1994 vol. 48 p. 385 - 389

0960-0760

Accumulated evidence indicates that the adrenal cortex is able to regulate prolactin (PRL) secretion in rats. The aim of this study was to determine the participation of adrenal steroids on the regulation of PRL release in ovariectomized (OVX) and oestrogen-treated rats, by using mifepristone or a specific progesterone antiserum. Blood samples were obtained at 13:00 and 18:00 h 3 days after priming with oestradiol benzoate (OB). A significant increase in serum PRL at 13:00 and 18:00 h was induced by OB treatment. The administration of mifepristone to OVX and oestrogen-primed rats enhanced serum PRL increase at 13:00 h, without modifying the values at 18:00 h; while the administration of progesterone antiserum did not modify PRL levels, indicating that the effect of mifepristone on PRL secretion is due to its antiglucocorticoid action. Adrenalectomy induced a release of PRL at 13:00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone administration. Treatment with a low dose of progesterone (0.1 mg/rat) to OVX, adrenalectomized and oestrogen-primed rats did not modify the effect of adrenalectomy in serum PRL. Progesterone (2 mg/rat) given at 08:00 h to OVX and oestrogen-primed rats increased serum PRL 5 h later. Mifepristone treatment partially reverted the PRL increase induced by progesterone. These results suggest that after a previous sensitization of the pituitary by oestrogen, circulating glucocorticoids may exert a direct inhibitory effect on PRL release. This inhibition takes place at 13:00 h on day 3. On the other hand, the lack of effect of mifepristone or adrenalectomy on the PRL release at 18:00 h may also indicate that neither progesterone nor glucocorticoids modify PRL release induced by oestrogen at this time.