During high salt (HS) diet the kidney increases urinary Na⁺ and volume excretion to match intake. We recently reported that HS provokes a redistribution of DCT NCC from apical to sub-apical vesicles as well as decreases NCC abundance. This study aimed to test the hypothesis that the other renal Na⁺ transporters' abundance and or subcellular distribution is decreased by high salt diet. Six wk Sprague Dawley rats were fed either a normal 0.4% NaCl diet (NS) diet or high salt 4% NaCl diet (HS) for 3 wks or overnight. Kidneys excised from anesthetized rats were fractionated on density gradients or analyzed by microscopy; transporters and associated regulators were detected with specific antibodies. Three week HS doubled Na⁺/H⁺ exchanger 3 (NHE3) phosphorylation at serine 552, and provoked a redistribution of NHE3, dipeptidyl peptidase IV (DPPIV), myosin VI, Na⁺ -Pi cotransporter type 2 (NaPi2), Angiotensin II type 2 receptor (AT₂R), aminopeptidase N (APN), Na-K-2Cl cotransporter (NKCC2), epithelial sodium channel (ENaC) subunit, Na,K-ATPase (NKA) 1 and 1 subunits from low density plasma membrane enriched fractions to higher density intracellular membrane enriched fractions. NHE3, myosin VI and AT₂R retraction to the base of the microvilli during HS was evident by confocal microscopy. HS did not change abundance of NHE3, NKCC, Na,K-ATPase 1 or 1 but increased ENaC in high density intracellular enriched membranes. Responses to HS were fully apparent after just 18 hr. We propose that retraction of NHE3 to the base of the MV, driven by myosin VI and NHE3 phosphorylation and accompanied by the redistribution of the NHE3 regulator DPPIV, contributes to a decrease in proximal tubule Na⁺ reabsorption during HS and that redistribution of transporters out of low density plasma membrane enriched fractions in the TALH and distal nephron may also contribute to the homeostatic natriuretic response to HS diet.