Eli Y. Adashi

The effect of acutely administered 2-hydroxyestrone on the release of gonadotropins and prolactin before and after estrogen priming in hypogonadal women.

Abstract Acute intraveneous administration of 2-hydroxyestrone (2-OHE 1 ; 250 and 500 μg) to hypogonadal women, resulted in no appreciable alterations in the circulating levels of LH, FSH and PRL. However, following a 5 day course of treatment with ethinyl estradiol (EE; 300 μg/day), progressive decrements (P 1 administration. PRL levels remained unaltered. It is concluded that 2-OHE 1 acutely administered to estrogen-primed hypogonadal women inhibits the release of both LH and FSH. It is thus possible that the transformation of estrogen to 2-OHE 1 may be involved in the feedback regulation of gonadotropin secretion.

The effect of estrogen priming of hypogonadal women on the release of gonadotropins and prolactin in response to 2-hydroxyestradiol

We have previously shown that the administration of a 2-hydroxyestradiol (20H-E2) infusion (250 microgram/h x 4 h) to hypogonadal women resulted in a selective increase in the levels of circulating prolactin (PRL) without changes in LH or FSH. The present study concerns the effect of estrogen priming of hypogonadal women on the release of gonadotropins and PRL in response to an identical 20H-E2 infusion. Estrogen priming consisted of a 5 day course of orally administered ethinyl estradiol at a daily dose of 300 micrograms. Significant (P less than 0.05) inhibition of LH release was observed within 1 h of the onset of the 20H-E2 infusion reaching a nadir (-25 +/- 2%) by 3.75 h. The circulating levels of FSH remained unaltered for the duration of the 8 h study. In contrast, significant (P less than 0.05) increments in the release of PRL could clearly be detected after a lag period of 1.5 h reaching a peak (+91 +/- 11%) by 4 h. These and previous findings demonstrate that the inhibitory influence of 20H-E2 on gonadotropin secretion is conditional upon prior estrogen priming while the ability of 20H-E2 to stimulate the release of PRL is not.