title: Significance of oestradiol for follicular development in hypogonadotrophic immature rats treated with FSH and hCG.
abstract: Administration of hCG (0.5 i.u.) to immature female rats that were made hypogonadotrophic by injections of an LHRH-antagonist at 22, 24, 26 and 28 days of age and in which follicular development was induced by FSH (10 i.u., given from day 26 until day 29) stimulates follicles to grow to their preovulatory size with a low amount of atresia. To investigate whether this effect of hCG on follicular growth is due to stimulation of oestradiol production, intraovarian concentrations of oestradiol were suppressed by an aromatase inhibitor and oestradiol action was blocked by an oestrogen antagonist; both of these were administered from day 25 until day 29. By day 30 this treatment had resulted in an increase in the percentage of atretic follicles. In turn, oestradiol benzoate (100 micrograms or 1000 micrograms day-1), given from day 26 until day 29 in rats treated with 10 i.u. FSH, resulted in (1) an increase in the total number of antral follicles, (2) an increase in follicular size and (3) a decrease in the percentage of atretic follicles. Although the administration of 1000 micrograms oestradiol benzoate can mimic the effects of 0.5 i.u. hCG on follicular growth to a large extent, the number of follicles with a diameter > 575 microns in rats treated with FSH plus oestrogen was smaller than that in rats treated with FSH plus hCG (10 +/- 2 and 24 +/- 2, respectively). Furthermore, a single injection of 10 i.u. hCG given on day 29 was used to induce ovulation: fewer ova were found in rats treated with FSH plus 1000 micrograms oestrogen than in rats treated with FSH plus hCG (15.2 +/- 2.1 and 46.5 +/- 1.6, respectively). From these studies, it is concluded that the effects of hCG on follicular growth and atresia can be largely attributed to the mitotic and anti-atretic effect of oestradiol. However, part of the effect of hCG cannot be explained on the basis of oestradiol action.
authors.affiliation: Department of Endocrinology and Reproduction, Faculty of Medicine and Health Sciences, Erasmus University, Rotterdam, The Netherlands.
authors.forename: J T
authors.initials: JT
authors.lastname: Uilenbroek
authors.forename: P
authors.initials: P
authors.lastname: Kramer
authors.forename: B
authors.initials: B
authors.lastname: Karels
authors.forename: F H
authors.initials: FH
authors.lastname: de Jong
mesh_terms: D000818:Animals; D047072:Aromatase Inhibitors; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D004958:Estradiol / Q000031:analogs & derivatives / Q000378:metabolism* / Q000494:pharmacology; D004965:Estrogen Antagonists / Q000494:pharmacology; D017316:Fadrozole / Q000494:pharmacology; D005260:Female; D005640:Follicle Stimulating Hormone / Q000494:pharmacology*; D000077267:Fulvestrant; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000494:pharmacology; D006727:Hormone Antagonists / Q000494:pharmacology; D007006:Hypogonadism / Q000378:metabolism / Q000503:physiopathology*; D007265:Inhibins / Q000378:metabolism; D006080:Ovarian Follicle / Q000187:drug effects / Q000502:physiology*; D010053:Ovary / Q000378:metabolism; D010060:Ovulation / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
chemical_list: D047072:Aromatase Inhibitors; D006063:Chorionic Gonadotropin; D004965:Estrogen Antagonists; D006727:Hormone Antagonists; D000077267:Fulvestrant; D007987:Gonadotropin-Releasing Hormone; D004958:Estradiol; D007265:Inhibins; C042691:LHRH, N-acetyl-(4-chlorophenylalanyl)(1)-(4-chlorophenylalanyl)(2)-tryptophyl(3)-arginyl(6)-alanine(10)-; D005640:Follicle Stimulating Hormone; D017316:Fadrozole