Oxidative stress and altered endothelial cell function in preeclampsia

Evidence continues to accumulate that oxidative stress is a mediator of endothelial cell dysfunction and thus contributes to the cardiovascular complications of preeclampsia. The mechanisms for the interaction of oxidative stress and endothelial cell function have not been well defined. This review explores potential vasoactive pathways that may be affected by oxidative stress and have been reported to be altered in women with preeclampsia. In pathologic conditions of oxidative stress, increased production of superoxide anions may be responsible for impairment of endothelial cell function. The interaction of superoxide anions and nitric oxide has been recognized to inactivate nitric oxide as it vasorelaxant as well as produce peroxynitrite, a potent oxidant. Increased prostaglandin H (PGH) synthase activity resulting in vasoconstriction predominates in models of oxidative stress. Peroxynitrite increases PGH synthase activity in vitro, providing a potential, but as yet untested, link between oxidative stress, nitric oxide, and the PGH synthase pathway leading to reduced relaxation and increased constriction in the vasculature of women with preeclampsia. Other vasoconstrictors (such as isoprostanes and endothelin) that may be interrelated with oxidative stress and altered endothelial cell Junction in preeclampsia are also discussed.