Blockage by Actinomycin D of Estradiol-17β-Induced Uterine Contractions in Ewes

Publisher Website
Google Scholar
Abstract
Actinomycin D, a blocker of DNA-dependent RNA synthesis, and estradiol-17β were injected into ovariectomized ewes in two experiments to determine whether estradiol-induced origination of contractions in the posterior uterus is mediated by increased RNA synthesis; i.e., genome activation. In Experiment I ewes had been ovariectomized 3 weeks before treatment. In Experiment II ewes were ovariectomized on Day 14 of the estrous cycle and treated on Day 15. Uterine contractions in both experiments were observed at 18 to 24 hr after treatment. Actinomycin D blocked the effect of estradiol on site of origination of contractions in both experiments. Of the total number of contractions observed in 10 min, the percentages originating in the posterior uterus in Experiment 1 (ewes ovariectomized 3 weeks before treatment) were: untreated, 22; actinomycin D, 16; estradiol, 75 and estradiol + actinomycin D, 17. The percentages in Experiment II (ewes ovariectomized on Day 14) were 31, 22, 70 and 22, respectively. In Experiment I, estradiol + actinomycin D did not significantly affect the total number of contractions observed in 10 minutes (average = 24). In Experiment II, estradiol reduced the total number of contractions observed in 10 min from 46 to 27. Actinomycin D blockage of the estradiol shift in the site of origin of uterine contractions to the posterior uterus was probably mediated by the effect of actinomycin D on RNA synthesis. In both experiments, estradiol aloneincreased the RNA/DNA ratio in endometrium and myometrium but the increase was less when given with actinomycin D. The effect of estrogen and actinomycin D on tissue water uptake was unlike their effects on uterine contractions. Estradiol increased water uptake in both experiments and was not blocked by actinomycin D. Copyright © 1978. American Society of Animal Science . Copyright 1978 by American Society of Animal Science

This publication has 0 references indexed in Scilit: