Prenatal Influences and Endothelial Dysfunction

Abstract

Hypertension during pregnancy when associated with new-onset proteinuria is termed “preeclampsia.”1,2 Preeclampsia is thought to initiate with improper remodeling of the uterine spiral arteries leading to reduced placental/fetal perfusion and subsequent extensive dysfunction of the maternal vascular endothelium.1,2 Reduced placental perfusion, however, may not always result in preeclampsia.1 Additionally, reduced placental perfusion may not necessarily reflect an imbalance between nutrient delivery and the metabolic needs of the fetus. Nonetheless, based on the fact that low placental perfusion is not always associated with preeclampsia, Roberts and Gammill1 proposed that the maternal response to reduced placental perfusion requires interaction with pre-existing maternal factors. Maternal factors that may contribute to increased maternal susceptibility to reduced placental perfusion and development of preeclampsia or hypertensive disorders of pregnancy include genetic, behavioral, and environmental factors.1 Numerous studies indicate that a genetic component may contribute to increased risk for preeclampsia and hypertensive disorders of pregnancy.1,3,4 Women and men born to a woman with preeclampsia are at greater risk for developing, or fathering, a preeclamptic pregnancy, suggesting transmission of a fetal gene for increased susceptibility to preeclampsia.3,4 However, this susceptibility is greater in women than in men, suggesting passage of maternal susceptibility …