Transcellular flux of urea across human placenta may be facilitated by aquaglyceroporins and/or by urea transporters (UT). Previously we have reported the presence of AQP3 and AQP9 in the syncytiotrophoblast of human term placenta (hST). In the present study, we detected a significant uptake of water, urea and mannitol sensitive to mercury and phloretin in explants from normal term placenta, which indicates a functional AQP9. In addition, we observed an increase of AQP9 expression in preeclamptic placenta with a lack of functionality of AQP9 for water and mannitol. Our data showed a molecular and functional expression of UT-A in hST from normal and preeclamptic placentas. In the last case, urea uptake sensitive to phloretin and mercury increased and the UT-A protein seems to be augmented. These results suggest that the increase of urea uptake in preeclamptic pregnancies could be attributed to an increase of expression of UT-A more than AQP9 proteins. In conclusion, our results provide new evidences that suggest the involvement of AQP9 and UT-A in the urea excretion mechanism across hST from mother to fetus in physiological conditions. Much further work is needed to define whether the overexpression of AQP9 plays a direct role either in the pathogenesis or in the adaptative response of preeclampsia.