Recent insights into the roles of nitric oxide and renin-angiotensin in the pathophysiology of preeclamptic pregnancy.
Review
Overview
abstract
Normal pregnancy involves marked maternal hemodynamic adaptations; these are suppressed in preeclampsia, leading to serious complications for mother and baby. The cause of preeclampsia is unknown, but may involve primary pathology at the maternal/fetal interface. However, the systemic manifestations of the disease are associated with widespread maternal vascular endothelial damage and dysfunction. There has been considerable recent interest in the possible roles for nitric oxide (NO) deficiency and for alterations in the renin angiotensin system (RAS) in the pathophysiology of preeclampsia. The following is an overview of the hemodynamic responses to normal pregnancy, an evaluation of the possible roles of NO and the RAS in these adaptations, and a review of the important aspects of these systems in preeclampsia.