MODULATION OF PROLACTIN, LUTEINIZING-HORMONE (LH) AND FOLLICLE-STIMULATING HORMONE (FSH) SECRETION BY LHRH AND BROMOCRIPTINE (CB154) IN THE HYPOPHYSECTOMIZED PITUITARY-GRAFTED MALE-RAT AND ITS EFFECT ON TESTICULAR LH-RECEPTORS AND TESTOSTERONE OUTPUT

Hypophysectomized adult male rats with a pituitary transplant under the kidney capsule were used to study the effects of chronic treatment with LHRH [luteinizing hormone-releasing hormone], with or without CB154, on the secretion of LH [lutropin], FSH [follitropin] and prolactin [PRL] and the action of these hormones on testicular LH receptors and testosterone [T] secretion. The presence of a pituitary transplant resulted in the expected increase in circulating levels of PRL. Treatment with LHRH (5 or 50 .mu.g) caused a significant increase in basal serum levels of FSH, but not LH, after 7 or 14 days of treatment. Treatment with CB154 reduced serum PRL levels, but did not affect the secretion of LH or FSH. The presence of a pituitary transplant alone increased testicular binding of hCG [human chorionic gonadotropin] without increasing testis weight. Administration of LHRH was associated with an increase in testis weight and with the capacity of the whole testis to bind hCG. Administration of CB154 to rats having transplants and receiving 5 .mu.g LHRH reduced testicular binding of hCG without affecting testis weight. Basal testicular T secretion in vitro was increased in all groups receiving pituitary transplants. hCG-stimulated T secretion in vitro was increased significantly over hypophysectomized controls only when gonadotropin secretion was maintained by LHRH treatment with or without CB154. Small amounts of LHRH stimulated a greater and more prolonged increase in the levels of FSH than of LH; something from the pituitary transplant, presumably PRL, induces or maintains LH receptors in the testis without affecting testis weight or hCG-stimulated T secretion in vitro; LHRH treatment and the increased gonadotropin secretion caused by it, increase testis weight with an associated increase in LH binding and ability to secrete T after hCG stimulation in vitro.