Preeclampsia, a major cause of maternal death and perinatal morbidity, strikes 1 in 20 pregnancies. Symptoms of preeclampsia include hypertension and proteinuria. Preeclampsia can progress to eclampsia, which is characterized by life-threatening brain seizures and kidney damage in the mother. Early delivery of the baby and placenta is the only currently available treatment for the disease. This treatment, however, leads to premature births and sometimes the baby's death. While previous studies have suggested that the placenta plays a central role in the pathogenesis of preeclampsia, the factors linking placental disease with cardiovascular and renal abnormalities are unclear. Thus, the identification of novel factors that link placental ischemia and maternal endothelial and vascular abnormalities in preeclampsia remains an important area of investigation. Experimental induction of chronic uteroplacental ischemia appears to be the most promising animal model to study potential mechanisms of preeclampsia since reductions in uteroplacental blood flow in a variety of animal models lead to a hypertensive state that closely resembles preeclampsia in women. We have developed a placental ischemia model to provide a better understanding of the physiological mechanisms which link low blood flow to placenta with cardiovascular abnormalities observed in preeclamptic women. Studies performed in several laboratories have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. In light of the recent developments in the understanding ofthe pathophysiology of preeclampsia, treatment strategies aimedat delaying the disease process and reducing maternal and perinatal morbidity are now being explored by many laboratories.