Isolated human placental cotyledons from normal term (37-40 weeks of gestation) and preterm (26-36 weeks of gestation) labor were perfused in vitro, and the effect of angiotensin II (ANG II) and its interaction with prostanoids was measured. In the preterm group, ANG II caused greater maximal increases in perfusion pressure than in normal term pregnancies without affecting sensitivity. Also, preparations from normal term pregnancies showed a marked development of tachyphylaxis compared to placentae from preterm pregnancies. Indomethacin (10(-6) M) increased the maximum pressor response to ANG II by 33.6% in normal term, however, in preterm placentas a 39.2% reduction was observed. Infused ANG II 10(-6) M) decreased the concentrations of thromboxane B(2) and 6-keto-PGF(1alpha) in both pregnancy groups, but this effect was not statistically different from the baseline values. In the current study, we show that the placenta of preterm pregnancies in basal conditions produce 7.6 times as much thromboxane as the normal term placenta (2,800+/-470 vs. 366.5+/-62 pg/min, respectively), without significant change in prostacyclin levels (preterm 88.6+/-11.0 vs. Term 100.6+/-30.7 pg/min). These observations provide evidence that the contribution of basally released thromboxane from placental tissue appears to contribute to abnormalities in the regulation of fetoplacental hemodynamics in premature pregnancies.