Twenty hyperprolactinemic patients with galactorrhea were studied to determine their gonadotropic responses to various stimuli. Five women lacked response to gonadotropin following the administration of clomiphene citrate. Ten patients who had luteinizing hormone releasing hormone (LRH) tests before and during bromocriptine administration exhibited varied FSH and LH responses that apparently were unaffected by bromocriptine therapy. A loss of the normal positive feedback of estrogens at the level of the hypothalamus was demonstrated in most patients before and during bromocriptine therapy. Long-term treatment with bromocriptine in 11 women resulted in a decrease of serum prolactin, cessation of lactation in all, and pregnancy in 8. These results suggest that the failure of normal secretion of gonadotropins in hyperprolactinemic women may result from 1) inadequate release of endogenous LRH, and 2) loss of the positive feedback of estrogens, as a result of the same hypothalamic disturbance that provokes the hyperprolactinemia. In turn, the elevated prolactin levels may exert a short-loop negative feedback at the hypothalamic level, inhibiting cyclic gonadotropin release.