When blood pressure (BP) is elevated above baseline, a pressure natriuresis-diuresis response ensues, critical to volume and BP homeostasis. Distal convoluted tubule Na⁺-Cl^- cotransporter (NCC) is regulated by trafficking between apical plasma membrane (APM) and sub-apical cytoplasmic vesicles (SCV). We aimed to determine whether NCC trafficking contributes to pressure diuresis by decreasing APM NCC or compensates for increased volume flow to the DCT by increasing APM NCC. BP was raised 50 mmHg (high BP) in rats by arterial constriction for 5 or 20-30 min provoking a 10 fold diuresis at both times. Kidneys were excised and NCC subcellular distribution analyzed by: 1) sorbitol density gradient fractionation and immunoblot and 2) immuno-electron microscopy. NCC distribution did not change after 5 min high BP. After 20-30 min high BP 20% of NCC redistributed from low density APM enriched fractions to higher density endosome enriched fractions and by quantitative immuno-EM, pool size of APM NCC decreased 14% and SCV pool size increased. Because of the time lag of the response, we tested the hypothesis that internalization of NCC was secondary to the decrease in angiotensin II (AngII) that accompanies high BP. Clamping AngII at a non pressor level by co-infusion of captopril (12 µg/min) and AngII (20 ng • kg ^-1 • min ^-1 ) during 30 min high BP reduced diuresis to 8 fold and prevented redistribution of NCC from APM to SCV enriched fractions. We conclude that DCT NCC may participate in pressure natriuresis-diuresis by retraction out of apical plasma membranes and that the retraction is, at least in part, driven by the fall in AngII that accompanies acute hypertension.