We tested the hypothesis that increased oxytocin is a necessary mechanism for the mediation of androstenedione (Δ4A)-induced myometrial contractions by investigating the effects of maternal treatment with the oxytocin antagonist atosiban on in vivo Δ4A-induced contractions. In four monkeys (group I), maternal estradiol, oxytocin, and myometrial contractions were assessed at baseline and after continuous iv Δ4A administration. Similar measurements were made in three monkeys (group II) that received the same Δ4A infusion regimen, but in addition were treated daily with atosiban. Maternal estradiol and oxytocin levels and contractions were also assessed in four additional monkeys (controls; group III), in which the Δ4A vehicle, intralipid, was infused iv continuously. In group I, Δ4A induced myometrial contractions and increased maternal estradiol and oxytecin to term concentrations. No myometrial contractions occurred in group II monkeys after combined Δ4A and atosiban treatment despite estradiol being elevated to concentrations similar to those measured in group I monkeys. Atosiban had no effect on maternal heart rate or blood pressure. Maternal estradiol, oxytocin, and number of myometrial contractions remained unchanged from baseline values in control monkeys. In conclusion, oxytocin is a necessary part of the mechanisms mediating Δ4A-induced myometrial contractions. Δ4A promotes myometrial contractions via similar mechanisms that mediate spontaneous term contractions in pregnant monkeys.
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