Angiotensin II (AngII) stimulates proximal tubule (PT) sodium and water reabsorption. We showed that treating rats acutely with the angiotensin converting enzyme inhibitor captopril decreases PT salt and water reabsorption and provokes rapid redistribution of the Na⁺/H⁺ exchanger isoform 3 (NHE3), Na⁺/Pi co-transporter 2 (NaPi2) and associated proteins out of the microvilli. The aim of the present study was to determine whether acute AngII infusion increases the abundance of PT NHE3, NaPi2 and associated proteins in the microvilli available for reabsorbing NaCl. Male Sprague Dawley rats were infused with a dose of captopril (12μg/min for 20min) that increased PT flow rate ~20% with no change in blood pressure (BP) or GFR. When AngII (20ng/kg/min for 20 min) was added to the captopril infusate PT volume flow rate returned to baseline without changing BP or GFR. After captopril, NHE3 was localized to the base of the microvilli and NaPi2 to sub-apical cytoplasmic vesicles; after 20 min AngII, both NHE3 and NaPi2 redistributed into the microvilli, assayed by confocal microscopy and density gradient fractionation. Additional PT proteins that redistributed into low density microvilli enriched membranes in response to AngII included: myosin VI, DPPIV, NHERF-1, ezrin, megalin, vacuolar H⁺-ATPase, aminopeptidase N, and clathrin. In summary, in response to 20min AngII in the absence of a change in BP or GFR, multiple proteins traffic into the PT brush border microvilli where they likely contribute to the rapid increase in PT salt and water reabsorption.