Nitric oxide and prostaglandin systems inhibition on the isolated perfused human placenta from normal and preeclamptic pregnancies.

Isolated human placental cotyledons from normal (NG) and preeclamptic gestants (PG) were perfused in vitro, and the effect of N omega-nitro-L-arginine (L-NA, 100 microM), methylene blue (MB, 50 microM), and indomethacin (INDO, 10 microM), on resting perfusion pressure and on the 5-hydroxytryptamine (5-HT)-induced vasoconstriction was established. In the HG, L-NA and MB increased resting perfusion pressure (p < 0.001) and INDO had no significant effect on resting pressure. In the PG, these agents did not significantly modify resting perfusion pressure. In the PG, 5-HT (10 microM-1 microM) caused greater maximal increases in perfusion pressure than in NG. In the NG, L-NA greatly enhanced the 5-HT-induced pressure, however INDO attenuated this effect. In the PG, L-NA did not modify significantly the 5-HT-induced response, but INDO reduced this response. These results suggest that basal release of nitric-oxide but not of vasodilator prostanoids may contribute to the low resting vascular tone in the NG and attenuates the strong vasoconstrictor effect induced by 5-HT. Impairment of action of nitric oxide could contribute to the enhanced pressor response to 5-HT observed in the PG.