Preeclampsia is associated with an increase of circulating levels of microparticles but their role in vascular dysfunction occurring during this disease is not understood yet. As this is a gestational disease, we tested the effect of microparticles from either preeclamptic women (PrMPs) or normal pregnant women (CMPs) on vessels from pregnant mice. For this purpose, the response to serotonin (5-HT) was tested on aortic rings from pregnant mice exposed 24 h to circulating levels of either PrMPs or CMPs. Interestingly, PrMPs but not CMPs were able to induce hyporeactivity in response to 5-HT in pregnant mice aortas. The NO-synthase inhibitor, N^G-nitro-L-arginine, strongly enhanced the response to 5-HT in vessels treated with PrMPs, but it had no significant effect on those treated with CMPs. Moreover, the selective cyclooxygenase-2 (COX-2) inhibitor, NS-398, completely abolished contraction to 5-HT in PrMPs-treated vessels whereas it only reduced response to the same agonist in vessels treated with CMPs, suggesting an increased participation of COX-2 vasoconstrictor products in the effect of PrMPs. In line with this hypothesis, PrMPs enhanced levels of both 8_Isoprostane and PGE₂ in vessels, despite reduction of thromboxane B₂. These results strengthen the main concept that microparticles in preeclampsia could act as vectors stimulating intracellular cascades in vascular cells leading to an enhanced NO production counteracting increased COX-2 vasoconstrictor metabolites by taking into account pregnancy.