Placental oxidative stress in malnourished rats and changes in kidney proximal tubule sodium ATPases in offspring

1 Intrauterine malnutrition has been linked to the development of adult cardiovascular and renal diseases, which are related to altered Na+ balance. Here we investigated whether maternal malnutrition increases placental oxidative stress with subsequent impact on renal ATP‐dependent Na+ transporters in the offspring. 2 Maternal malnutrition was induced in rats during pregnancy by using a basic regional diet available in north‐eastern Brazil. Placental oxidative stress was evaluated by measuring thiobarbituric acid‐reactive substances, which were 35–40% higher in malnourished dams (MalN). Na+ pumps were evaluated in control and prenatally malnourished rats (at 25 and 90 days of age). 3 Identical Na+/K+‐ATPase activity was found in both groups at 25 days (approximately 150 nmol Pi/mg per min). However, although Na+/K+‐ATPase increased by 40% with growth in control rats, it remained constant in pups from MalN. 4 In juvenile rats, the activity of the ouabain‐insensitive Na+‐ATPase was higher in MalN than in controls (70 vs 25 nmol Pi/mg per min). Nevertheless, activity did not increase with kidney and body growth: at 90 days, it was 50% lower in MalN than in controls. The maximal stimulation of the Na+‐ATPase by angiotensin (Ang) II was 35% lower in MalN than in control rats and was attained only with a much higher concentration of the peptide (10−10 mol/L) than in controls (10−14 mol/L). 5 Protein kinase C activity, which mediates the effects of AngII on Na+‐ATPase was only one‐third of normal values in the MalN group. 6 These results indicate that placental oxidative stress may contribute to fetal undernutrition, which leads to later disturbances in Na+ pumps from proximal tubule cells.