Abstract
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 a 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 function in preeclampsia are also discussed.
Keywords:
Oxidative stress - free radical - endothelial cell - vascular - preeclampsia
