The role of PRL in the control of corpus luteum (CL) function was examined in hyperprolactinemic and euprolactinemic female rhesus monkeys with hypothalamic lesions in which ovulatory menstrual cycles were induced by the pulsatile administration of GnRH, in intact postpartum monkeys nursing their infants, as well as in animals treated with bromocriptine. In the lesioned monkeys, neither markedly elevated nor undetectable (bromocriptine-suppressed) PRL levels influenced the time courses of postovulatory plasma progesterone concentrations compared to those in monkeys with normal PRL concentrations. Plasma progesterone concentrations in the hyperprolactinemic monkeys, however, did not decline to undetectable levels at the end of the luteal phase, as is the case in normal animals, but remained slightly elevated for extended periods, a pattern characteristic of lactating animals. In both lesioned and postpartum animals, bromocriptine administration or removal of suckling infants from the latter resulted in complete functional luteolysis. These observations suggest that PRL does not play a significant role in the control of the CL of the menstrual cycle, but that in high concentrations, this hormone can partially maintain previously established CL.