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High salt, Ang II (angiotensin II), and reactive oxygen species enhance progression of chronic kidney disease. We tested the hypothesis that a high salt intake generates specific reactive oxygen species to enhance Ang II contractions of afferent arterioles from mice with reduced renal mass (RRM). C57BL/6 mice were subjected to surgical RRM or sham operations and received 6% or 0.4% NaCl salt diet for 3 months. Ang II contractions were measured in perfused afferent arterioles and superoxide (O 2  - ) and hydrogen peroxide (H 2 O 2 ) by fluorescence microscopy. RRM enhanced the afferent arteriolar gene expression for p47 phox and neutrophil oxidase (NOX) 2 and high salt intake in RRM mice enhanced gene expression for angiotensin type 1 receptors, POLDIP2 and NOX4 and reduced catalase. High salt in mice with RRM enhanced arteriolar O 2  - and H 2 O 2 generation and maximal contractions to Ang II (10 -6 mol/L) that were dependent on O 2  - because they were prevented by gene deletion of p47 phox and on H 2 O 2 because they were prevented by transgenic smooth muscle cell expression of catalase (tg CAT-SMC ) and POLDIP2 gene deletion. Three months of tempol normalized arteriolar reactive oxygen species and Ang II contractions. However, arteriolar contractions to lower concentrations of Ang II (10 -8 to 10 -11 mol/L) were paradoxically inhibited by H 2 O 2 and POLDIP2. In conclusion, both O 2  - from p47 phox /NOX2 and H 2 O 2 from NOX4/POLDIP2 enhance maximal arteriolar Ang II contractions from RRM mice during high salt, but H 2 O 2 and NOX4/POLDIP2 reduce the sensitivity to lower concentrations of Ang II by &gt;100-fold. Tempol prevents all of these changes in function.

High Salt Enhances Reactive Oxygen Species and Angiotensin II Contractions of Glomerular Afferent Arterioles From Mice With Reduced Renal Mass