Abstract
Adrenocorticotropin (ACTH), dehydroepiandrosterone (DHA) and dexamethasone increase urinary estrogens when given to normal subjects during the follicular phase of the menstrual cycle; however, there is no estrogen stimulation by these agents when given during the luteal menstrual phase. In addition to this relationship between menstrual phase and estrogen stimulation, the urinary estrogen response to ACTH in oophorectomized subjects is quantitatively less than and qualitatively different from that of normal females given ACTH, which suggests that the principal source of urinary estrogens following ACTH stimulation of normal subjects is ovarian, not adrenal. ACTH stimulation of urinary estrogens is not a direct effect of ACTH but is mediated by a nonglucocorticoid product of adrenal stimulation. DHA has been shown to simulate ACTH augmentation of urinary estrogens and may be a mediator of adrenocortical influences on ovarian estrogen metabolism. For reasons discussed in the text, it is tentatively concluded that the observed urinary estrogen elevations following ACTH and DHA are a reflection of stimulated ovarian estrogen secretion rather than increased renal clearance or altered estrogen catabolism.