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Preeclampsia is associated with an imbalance between oxidants and antioxidants, resulting in reduced effects of the endothelium-derived, relaxing-factor nitric oxide (NO). Antioxidants, like N-acetylcysteine (NAC), remove reactive oxygen species, resulting in an improvement of endothelial function. We aimed to investigate the effect of NAC on the NO-pathway in the human fetoplacental circulation in preeclampsia and control pregnancies.The NO-pathway was investigated by use of the NO-synthase inhibitor L-NAME in an ex vivo cotyledon perfusion model.At baseline, fetoplacental arterial pressure was comparable in preeclamptic pregnancies (n = 8) and control pregnancies (n = 8), and increased dose-dependently after L-NAME. The maximal L-NAME–induced rise in fetoplacental arterial pressure was attenuated in preeclamptic versus control pregnancies (20.8 ± 2.0 mm Hg vs 36.7 ± 3.5 mm Hg, P < .05). Addition of NAC increased the L-NAME–induced rise in fetoplacental arterial pressure to 36.4 ± 3.4 mm Hg in preeclampsia pregnancies (P < .05) and to 49.2 ± 2.6 mm Hg in control pregnancies (P < .05).Preeclampsia is associated with a dysfunction of the NO-pathway. N-acetylcysteine increases NO-mediated effects in the fetoplacental circulation in preeclamptic placentas as well as in healthy control placentas.