Pregnant rats maintained on sodium overload shows reduced type‐1 VEGF receptor in placenta

Abstract

Sodium overload during pregnancy compromises the renal function of offspring at adult life. In this work we investigated whether maternal sodium overload affects placental lipid peroxidation and type‐1 VEGF receptor (VEGFR‐1) in the placenta. Pregnant Wistar rats were maintained with sodium chloride 1.8%, instead drinking water, from 20 days before pregnancy until the 20th day of pregnancy. Part of them was treated with α‐tocopherol or tempol from the 1st day of pregnancy. Maternal sodium overload did not change the placental or hepatic fetal lipid peroxidation; however it decreased the expression of VEGFR‐1 in placental labyrinth. Treatment with α‐tocopherol or tempol prevented sodium overload‐induced reduction in placental expression of VEGFR‐1. Different from tempol, α‐tocopherol effect was accompanied by reduction of lipid peroxidation in maternal placenta and fetal liver. These findings indicate that intrauterine programmed renal dysfunction produced by sodium overload might be due to compromised placental angiogenesis that is not correlated to placental lipid peroxidation. CAPES, CNPq and FACEPE.