Abstract
Hypophysectomized or intact immature female rats were given follicle-stimulating hormone (FSH), pregnant mare's serum gonadotrophin (PMS), human chorionic gonadotrophin (HCG), or luteinizing hormone (LH) for 3 days, with or without prior administration of diethylstilbestrol for 2 days. Priming with estrogen augmented the ovarian weight response produced by FSH or PMS in both hypophysectomized and intact animals. In contrast, estrogen pretreatment enhanced ovarian growth in intact rats given HCG or LH, but not in hypophysectomized animals similarly treated. Longer periods of priming also failed to augment the ovarian response to HCG in hypophysectomized rats. The ovaries of intact rats given diethylstilbestrol and FSH contained many corpora lutea, whereas luteinization was never noted in hypophysectomized animals similarly treated. Ovarian weight augmentation in the latter was due to enhanced follicular growth throughout the ovary. Estrogen and HCG produced cystic, luteinized follicles in intact rats, in contrast to the lack of such follicular stimulation in hypophysectomized animals. It is concluded that estrogen increases the ovarian response to gonadotrophins by 1) directly stimulating granulosal proliferation, and 2) effecting the release of endogenous gonadotrophins from the pituitary gland.
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