Preeclampsia is a disease characterized by hypertension and proteinuria but can manifest many abnormalities. Some of the best documented alterations involve changes in the handling of sodium ion both on the systemic and on the cellular level. There is broad agreement that the components of the renin-angiotensin-aldosterone pathway are markedly reduced in women with preeclampsia. However, other changes, especially those involving cell sodium are less consistent. A majority of studies support an increase in peripheral cell sodium concentration. This would suggest a defect in (Na,K)ATPase or sodium pump activity. Direct study of cellular sodium pump activity provides suggestive but not unequivocal support for this decreased sodium pump activity. Other evidence indicates increased circulating concentrations of a sodium pump inhibitor in most, but not all, studies of preeclampsia. Together, current research argues more strongly in favor of derangements of cell sodium handling perhaps mediated by circulating sodium pump inhibitors leading often to increased cell sodium. Such an increase of cell sodium in vascular tissue has previously been shown to enhance vascular sensitivity to vasoconstrictor agents or lead directly to increased vasoconstriction.