Pre-eclampsia (PE) is a leading cause of maternal hypertension in pregnancy and is associated with fetal growth restriction, premature birth, and fetal and maternal mortality. Activation and dysfunction of the maternal and fetal endothelium in PE appears to be a consequence of increased oxidative stress, resulting from elevated levels of circulating lipid peroxides. Accumulating evidence implicates reactive oxygen species (ROS) in the pathogenesis of vascular dysfunction in PE, perhaps involving a disturbance in intracellular Ca(2+) signaling. Several ion-transport pathways are highly sensitive to oxidative stress, and the resulting modulation of ion transport by ROS will affect intracellular Ca(2+) homeostasis. We review the evidence that changes in ion transport induced by ROS may be linked with abnormalities in Ca(2+)-mediated signal transduction, leading to endothelial and smooth muscle dysfunction in maternal and fetal circulations in PE. As dysregulation of Ca(2+) signaling in fetal umbilical endothelial cells is maintained in culture and embryonic, fetal, and postnatal development is affected by the cellular redox state, we hypothesize that impaired redox signaling in PE may influence "programming" of the fetal cardiovascular system and endothelial function in adulthood.