Cycloheximide Blockage of Estradiol-17β - Induced Contractions in Ovariectomized Ewes

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Abstract
The site of origin of uterine contractions was studied in 4 groups of ovariectomized ewes 24 h after the following treatments: none, 250 mg of cycloheximide, 45 .mu.g of estradiol or 45 .mu.g of estradiol + 250 mg of cycloheximide. In nontreated ewes, most contractions originated near the utero-tubal junction and moved caudally. In ewes treated with estradiol, most contractions originated in the posterior part of the uterus and moved cranially. In ewes treated with either cycloheximide alone or estradiol + cycloheximide, contractions originated near the utero-tubal junction and moved caudally, thus, cycloheximide blocked the estradiol-induced shift in the site of origin of contractions. Cycloheximide also reduced estradiol-induced increases in protein/DNA and RNA/DNA ratios. In a separate experiment with the same 4 treatment groups, the effects of estradiol and cycloheximide were determined on uterine concentrations of the contraction-stimulating agents prostaglandin F2.alpha. (PGF2.alpha.), prostaglandin E2 (PGE2) and norepinephrine. Estradiol alone did not have a measurable effect on the prostaglandin concentrations. Cycloheximide increased both PGF2 and PGE2 concentrations in endometrium and myometrium. The increase due to cycloheximide treatment was greater for the endometrium than for myometrium for both prostaglandins. Estradiol did not alter norepinephrine concentration significantly in the myometrium. Cycloheximide reduced myometrial norepinephrine concentrations whether or not estradiol has been coadministered. Estradiol probably does not regulate the site of origin of contractions in the uterus by modification of tissue concentrations of these contraction-stimulating agents as seen at 24 h after estradiol administration.

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