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Stimulation of renal sodium transporters’ abundance and phosphorylation during chronic angiotensin II (AII) infusion requires intrarenal AII formation

The hypertensive response to AII infusion (400ng/kg/min for 14 d) is blunted in mice expressing normal systemic ACE levels but no kidney ACE (ACE 10/10) vs. WT mice: mean arterial pressure increased 28 mmHg in ACE 10/10 mice vs. 42 mmHg in WT mice (p<0.001). Kidney AII content was also reduced 50% in AII infused ACE 10/10 vs. WT (p<0.05), (Gonzalez‐Villalobos, 2011). We tested the hypothesis that the reduced hypertensive response to AII infusion in the ACE 10/10 mice was due to blunted increases in renal Na+ transporters’ abundance or phosphorylation (‐P) along the nephron. Na+ transporter abundance was measured in whole kidney homogenates by immunoblotting. Density values in AII infused mice were normalized to values in uninfused WT and ACE10/10 mice defined as 1.00.