Pituitary Sensitivity to LHRH in Hyperprolactinemia Induced by Perphenazine and Renal Pituitary Transplants in Female Rats1

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Abstract
Considerable controversy exists as to the site of action of prolactin [P] in the attenuation of gonadotropin secretion. Therefore, the basal levels of serum FSH [follitropin] and LH [lutropin] and the response to LHRH [luteinizing hormone-releasing hormone, luliberin] were measured in intact, acutely and chronically ovariectomized rats with or without hyperprolactinemia. Hyperprolactinemia was induced by perphenazine treatment and pituitary transplants under the kidney capsule. The LHRH challenge was performed on day 6 of hyperprolactinemia. P levels induced by perphenazine were 4-5 times those induced by pituitary grafts. Ovariectomy produced a significant decrease in serum P levels in hyperprolactinemic animals. Intact and castrated perphenazine-treated animals had significantly depressed basal serum LH and FSH levels while only intact pituitary-grafted rats had significantly lower basal LH levels. In intact animals in which hyperprolactinemia was induced by either method, the pituitary LH response to LHRH was significantly depressed. In castrated rats, responsiveness to LHRH was unaltered with the pituitary transplant and unaltered or increased with perphenazine treatment. The modulatory effect of ovarian steroids on pituitary sensitivity to LHRH seems to be the primary mechanism by which the prolactin levels induced by 1 ectopic pituitary can reduce LH secretion. Experiments with perphenazine treatment in castrated rats which showed lower basal LH and unaltered or increased pituitary responsiveness to exogenous LHRH suggest decreased LHRH release by the hypothalamus.