Effect of median eminence lesions and hormonal replacement on the prolactin receptors in the adrenal gland and Langerhans islets from ovariectomized adult rats.

The effect of hyperprolactinemia induced by median eminence lesions (MEL) and ACTH and glucocorticoid replacement on prolactin (Prl) receptors was studied in the adrenal, isolated Langerhans islets and the liver. Adult rats were ovariectomized 15 days before MEL and they were divided in the following groups: 1) SHAM: injected with saline solution 3 times in alternate days; 2) MEL: saline solution; 3) MEL + ACTH: 50 micrograms: 10 IU/rat, s.c. (Synacthen) and 4) MEL + DEXA: 10 micrograms/rat (dexamethasone). For measuring total lactogenic binding sites an in vitro treatment of the membrane fraction with 4M MgCl2 was used. MEL originated a significant increase in Prl serum levels, which was not altered by injections of ACTH or dexamethasone. In contrast, serum corticosterone (B) levels in MEL rats were significantly lowered, and it was restored by ACTH. Unexpectedly, B levels increased when dexamethasone was administered to MEL rats. Prl receptors were diminished in the adrenal gland and Langerhans islets from MEL animals, as compared with the SHAM group. ACTH and glucocorticoid administration did not affect the pancreatic Prl receptors, while the adrenal gland exhibited a further lowering of Prl binding sites during ACTH treatment. Since no effect was found when dexamethasone was injected, a possible direct action of ACTH is suggested. On the other hand, Prl receptors were induced in the liver by MEL, and this action was abolished by dexamethasone and ACTH. Binding affinity in every tissue studied remained unchanged. Our data suggest that endogenous Prl is able to regulate its own receptors not only in the liver, but also in the adrenal gland and pancreatic islets.