Preeclampsia remains a major health problem for mothers and infants. Studying the entire pathophysiology of preeclampsia rather than "pregnancy-induced hypertension" has greatly expanded our knowledge of the disorder. Current thinking approaches preeclampsia as a 2 stage disorder: reduced placental perfusion usually secondary to abnormal implantation and a consequent maternal disorder characterized by endothelial dysfunction and subsequent pathophysiological changes. We know much about the 2 stages and less about their linkage. It is evident that reduced placental perfusion is not sufficient to account for the pathophysiology. Reduced perfusion and abnormal implantation occur in other conditions (intrauterine growth restriction and preterm labor) without the maternal syndrome. This leads to the hypothesis that reduced placental perfusion must interact with maternal constitutional factors to generate the systemic pathophysiology of preeclampsia. The similarities of these risk factors and metabolic alterations between preeclampsia and atherosclerosis suggest a common pathophysiology. Oxidative stress is postulated as the genesis of endothelial dysfunction in atherosclerosis. The author proposes that oxidative stress secondary to reduced placental perfusion leads to endothelial dysfunction, linking the 2 stages of the syndrome.