Renal redox response to normal pregnancy in the rat.

Normal pregnancy involves increased renal sodium reabsorption, metabolism, and oxygen consumption, which can cause increased oxidative stress (OS). OS can decrease nitric oxide (NO) bioavailability and cause pregnancy complications. In this study we examined the NO synthases (NOS) and redox state in the kidney cortex and aorta in early (E), mid (M), and late (L) pregnant (P) (days 3, 12, 20) and 2-4 days postpartum (PP) rats compared with virgin rats (V). Protein abundance of endothelial NOS (eNOS) was unchanged and neuronal NOS (nNOS)α fell at LP in the kidney cortex. Kidney cortex nNOSβ was elevated at MP, LP, and PP. No changes in aortic NOS isoforms were observed. Kidney cortex nitrotyrosine (NT) abundance decreased in EP, MP, and PP, whereas aortic NT increased in EP, MP, and PP. The NADPH oxidase subunit p22phox decreased in the kidney cortex at EP while aortic p22phox increased in EP and LP. No changes in kidney cortex NADPH-dependent superoxide production or hydrogen peroxide levels were noted. Kidney cortex cytosolic (CuZn) superoxide dismutase (SOD) was unchanged, while mitochondrial SOD decreased at EP and extracellular SOD decreased at MP and LP in the kidney cortex. Despite falls in abundance of kidney cortex SODs, total antioxidant capacity (TAC) was elevated in EP, MP, and PP in the kidney cortex. Aortic CuZn SOD deceased at PP, while the other aortic SODs and aortic TAC did not change. Data from this study suggest that the kidney cortex is protected from OS during normal rat pregnancy via an increase in antioxidant activity.