Estradiol-induced follicular atresia in rhesus monkeys is not prevented by exogenous gonadotropins.

Estradiol-17β (E2) induces atresia of the dominant preovulatory follicle (DF) when administered on day 6 of the menstrual cycle. The present study was designed to determine whether the atretogenic effect of E2 could be averted by the administration of exogenous gonadotropins, in an attempt to determine whether E2-induced atresia in primates is due to a direct action at the ovarian level or is mediated via pituitary secretion. After identification of the DF during laparoscopy, cyclic monkeys received Silastic capsules containing E2 placed s.c. for 24 hours, plus one of the following treatments: phosphate-buffered saline, or 25 I.U. of either human urinary menopausal gonadotropin (hMG), FSH-rich hMG, human urinary FSH (uFSH), or human pituitary FSH (pFSH) injected i.m. twice daily for 2 days. The control treatment resulted in atresia of the DF and extended follicular phases (26.3 ± 5.9 days, x̄ ± S.D.), but in normal luteal phases following ovulation of a substitute DF. Similar results occurred in all animals receiving FSH-rich hMG or pFSH, and in 11 of 16 animals receiving hMG or uFSH (P > 0.05). Since all possible routes and regimens of gonadotropin administration were not attempted, a central action of E2 cannot be ruled out. However, we believe that the experimental observations support our contention that the atretogenic action of E2 is exerted in part at the ovary.