Estradiol regulation of the frequency and site of origin of uterine contractions in news.
Five experiments were conducted to study the action of estradiol in regulating the frequency and site of origin of contractions in ewes anesthetized with sodium pentobarbitol. Contractions were observed visually by means of midventral laparotomy. In Exp. 1, the percentage of posterior contractions (contractions originating caudal to external bifurcation) of uterine horns and RNA/DNA declined by 36 to 48 hr after the onset of estrus; estradiol posterior contractions and increased RNA/DNA. In Exp. 2, the frequency of contractions in ovariectomized ewes was maximal (53 +/- 5) at 12 hr after an injection of 45 microgram estradiol and was about double the control value (28 +/- 9). The percentage of posterior contractions was greatest at 18 hr (90 +/- 5) and was almost nine times as great as control values (12 +/- 7). RNA/DNA increased from .26 +/- .07 at 12 hr to .48 +/- .05 at 18 hours. In Exp. 3, estradiol increased the frequency of contractions in ovariectomized ewes (48 +/- 2 vs 32 +/- 3) within 6 hours. Neither phenoxybenzamine nor cycloheximide blocked this estradiol-induced increase. In Exp. 4, estradiol increased the percentage of posterior contractions in ovariectomized ewes at 24 hr (7 +/- 4 vs 78 +/- 12), but not the frequency (24 +/- 5 vs 24 +/- 4). Neither 6-OH dopamine nor reserpine altered the estradiol effect on posterior origination of contractions, although reserpine reduced myometrial concentration (nanogram/milligram DNA) of norepinephrine (205 +/- 31 vs 52 +/- 16 without estradiol and 127 +/- 30 vs 62 +/- 13 with estradiol). In Exp. 5, estradiol increased the percentage of posterior contractions in ovariectomized ewes at 24 hr (8 +/- 4 vs 86 +/- 7), and the increase was blocked by indomethacin. Estradiol increased prostaglandin F (PGF) in endometrium but not in myometrium. Indomethacin reduced PGF in both tissues and blocked the estradiol-induced increase. Anterior portions of the uterus had higher concentrations of PGF than did posterior portions. Estradiol induction of high-frequency uterine contractions is dissociable from estradiol induction of a posterior site of origin of contractions, i.e., time for the two effects to appear in ovariectomized ewes differs and the estrogenic regulation of the site of origin of uterine contractions requires protein synthesis.
D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology*; D004971:Estrus; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D009638:Norepinephrine / Q000096:biosynthesis; D011247:Pregnancy; D011460:Prostaglandins F / Q000096:biosynthesis; D012110:Reserpine / Q000494:pharmacology; D012756:Sheep / Q000378:metabolism / Q000502:physiology*; D014590:Uterine Contraction / Q000187:drug effects*; D014599:Uterus / Q000378:metabolism
D011460:Prostaglandins F; D004958:Estradiol; D012110:Reserpine; D003513:Cycloheximide; D004298:Dopamine; D009638:Norepinephrine; D007213:Indomethacin