Differential Inhibition by Cortisol of Estrogen-Stimulated Uterine Responses

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Abstract
The ability of cortisol to block estrogen action in the uterus of the ovariectomized rat was studied 6 hr. after treatment with 0.2 ng estradlol-17[beta]. The estrogen-Induced increases in uterine weight, Na and Cl concentration, and a decline in K concentration, were blocked by the administration of 3 mg cortisol to each rat while the increase in water content was partially suppressed. The 3-fold increase in glycogenesis produced by estradiol was depressed by cortisol to a 2-fold increase over control glycogen content. The increase in free glucose concentration in the uterus which estrogen produces was blocked by cortisol, however. Uterine vascular permeability, measured quantitatively with trypan blue, doubled with estrogen, and cortisol did not block this increase. These separate effects of estradiol on water, electrolyte and glucose influx, as compared to trypan blue permeability and glycogen synthesis, demonstrate that several estrogenic end-points are independent of each other and are differentially inhibited by cortisol.