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

Estradiol‐17β (E 2 ) 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 E 2 could be averted by the administration of exogenous gonadotropins, in an attempt to determine whether E 2 ‐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 E 2 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 E 2 cannot be ruled out. However, we believe that the experimental observations support our contention that the atretogenic action of E 2 is exerted in part at the ovary.