High salt intake exacerbates renal tissue oxidative stress and urinary angiotensinogen excretion during AngII‐dependent hypertension.

Abstract

High salt (HS) intake inhibits systemic and intrarenal RAS; however, when AngII is not suppressed HS exacerbates hypertension and renal injury. We investigated the effects of HS on the magnitude of intrarenal oxidative stress associated with angiotensinogen urinary excretion (uAGT) in chronic AngII‐infused rats. In Sprague‐Dawley rats: 1) Control, normal salt diet [NS, n=5]; 2) HS diet [8% NaCl, 12 d, n=5]; 3) AngII‐infused in NS rats [AngII, 80 ng/min, 14 d, n=5] and 4) AngII‐infused in HS rats [AngII+HS, n=5] we measured systolic blood pressure (SBP), proteinuria, NADPH oxidase activity, n‐Tyr residues and uAGT. HS alone did not change SBP, but led to hypertension when combined with AngII. In contrast, HS alone led to proteinuria that was further increased in HS+AngII rats. The uAGT excretion rates increased in AngII+HS rats compared to AngII rats (AngII=107±18 vs AngII+HS=4363±1296 ng/day). Renal tissue oxidative stress measured by n‐Tyr Western blot increased in both HS and AngII+HS rats; however the NADPH oxidase activity increased only in HS+AngII rats (HS=10,674±2819; AngII+HS=18,663±1328 RLU/mg protein). HS exacerbates renal tissue oxidative stress during AngII‐dependent hypertension which might be associated with increased uAGT, proteinuria, and blood pressure in AngII‐infused rats.NIH [IdeA Program (P20RR01765906); Tulane‐BIRCWH Program (K12HGO4351)] and AHA (09PRE2209079; 09BGIA2280440)