The Mechanism of the Inhibition of Uterotrophic Responses by Acute Dexamethasone Pretreatment*

Paul S. Campbell
In: Endocrinology · 1978 · vol. 103(3) , pp. 716–723 · doi:10.1210/endo-103-3-716 · W2167131107
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Abstract

The mechanism of glucocorticoid antagonism of estradiol-stimulated uterotrophic responses was studied. Dexamethasone was administered sc at a dosage of 1000 μg 20–25 min before an injection of 1 μg estradiol. Uterine weights were measured at 3 and 24 h, and the quantity of nuclear-bound receptor-estrogen complex (REC) was determined at 1 and 6 h using the nuclear exchange assay. Additionally, uteri were incubated in Eagle's medium containing 10-8 M [3H]estradiol, either after an in vivo, or simultaneously with an in vitro, exposure to dexamethasone, and the quantity of nuclear-bound [3H]estradiol and total tissue uptake of [3H]estradiol were determined. Dexamethasone significantly reduced both 3- and 24-h uterine weights, with the early fluid imbibition being the more sensitive. This correlated with the dexamethasone-induced reduction in nuclear REC observed at 1 and 6 h after estradiol injection. Exposure of uteri either in vitro or in vivo to dexamethasone inhibited both nuclear bound and total tissue uptake of [3H]estradiol in vitro. However, the reduction in total tissue uptake of [3H]estradiol was greater than could be accounted for solely by the reduction in nuclear REC. Hence, it is proposed that dexamethasone acts to impair estrogen-induced growth of reproductive tissue indirectly. This impairment occurs at the level of the genome through reduction of nuclear REC as a result of restriction of transport of estradiol into uterine cells. Dexamethasone administration at various times after estradiol injection also reduced long term uterine growth. As dexamethasone antagonism of uterotrophic responses is evident even when the hormone is administered at times after the critical nuclear REC retention time necessary for eliciting long term growth, the reduction in nuclear REC is probably compounded by direct effects upon enzyme activity to impair uterine responsivity.

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