Abstract
The parturient uterus develops a markedly enhanced sensitivity to the uterotonic action of oxytocin (OT). The mechanism leading to this enhanced OT sensitivity is not known. Apparently prostaglandins (PG) may be involved. To define the relationship between OT sensitivity and uterine PG production, uterine sensitivity to OT was measured by a quantitative dose-response procedure in rats on days 19, 20, 21 and 22 of pregnancy and monitored uterine and placental tissue concentrations of PGF2.alpha. and PGE2. The effects of inhibition of endogenous PG synthesis on OT sensitivity and uterine contractility were determined. Both OT sensitivity and spontaneous contractility are positively related to uterine PGF2.alpha. production. An abrupt increase in OT sensitivity was observed on days 21 and 22 of pregnancy. The increase in OT sensitivity was coincidental with the marked increase in PGF2.alpha. production in the uterus on days 21 and 22 of pregnancy. Suppression of in vivo PG synthesis caused a reduction in both spontaneous uterine contractility and OT-induced contractions. Uterine PGE2 concentrations and release were 3-5 times lower than PGF2.alpha.. There were no significant fluctuations of uterine PGE2 concentration measured on these last 4 days of gestation. Placental PG levels were also not related to uterine contractility. Placental PGE2 levels were higher than PGF2.alpha. and may play a regulatory role in placental perfusion. However, placental PG did not vary with gestational age.