New Insights into the Pathogenesis and Treatment of Preeclampsia Based on Placental Aminopeptidases in Maternal Blood

The reduced uterine perfusion pressure model in pregnant rats closely mimics the pathophysiology of preeclampsia. Preeclampsia frequently occurs in high-altitude populations. Evidence suggests that fetal hypoxia is involved in the pathogenesis of preeclampsia. We proposed that the crosstalk between fetal angiotensin II (Ang-II) and vasopressin, and their degrading aminopeptidases (APs) in both the placenta and maternal blood, regulates placental circulation. Therefore, changes in maternal blood AP levels may reflect changes in placental circulation. Our present review contributes to the understanding of dynamic changes in placental circulation in preeclampsia and suggests that the pathophysiology of preeclampsia can be interpreted as a disturbance in the redistribution of blood flow to the placenta under fetal hypoxia. Furthermore, changes in APs in maternal blood may help explain two longstanding concepts in preeclampsia research: changes in responses to exogenous Ang-II and placental perfusion in preeclampsia. These findings also highlight the potential of placental APs as a future therapeutic target for preeclampsia.