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Effects of dietary salt on renal Na⁺ transporter subcellular distribution, abundance, and phosphorylation status

¹Department of Physiology and Biophysics, University of Southern California Keck School of Medicine, Los Angeles, California; and ²Water and Salt Research Center, Department of Cell Biology, Institute of Anatomy, University of Aarhus, Aarhus C, Denmark

Submitted 2 April 2008 ; accepted in final form 18 July 2008

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 distal convoluted tubule Na⁺-Cl^– cotransporter (NCC) from apical to subapical vesicles and decreases NCC abundance. This study aimed to test the hypothesis that the other renal Na⁺ transporters' abundance and or subcellular distribution is decreased by HS diet. Six-week-old Sprague-Dawley rats were fed a normal (NS) 0.4% NaCl diet or a HS 4% NaCl diet for 3 wk 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 (NHE)3 phosphorylation at serine 552 and provoked a redistribution of NHE3, dipeptidyl peptidase IV (DPPIV), myosin VI, Na⁺-P_i cotransporter (NaPi)-2, ANG II type 2 receptor (AT₂R), aminopeptidase N (APN), Na⁺-K⁺-2Cl^– cotransporter (NKCC2), epithelial Na⁺ channel (ENaC) β-subunit, and Na⁺-K⁺-ATPase (NKA) ₁- and β₁-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 (MV) during HS was evident by confocal microscopy. HS did not change abundance of NHE3, NKCC, or NKA ₁- or β₁-subunits but increased ENaC-β in high-density intracellular enriched membranes. Responses to HS were fully apparent after just 18 h. We propose that retraction of NHE3 to the base of the MV, driven by myosin VI and NHE3 phosphorylation and accompanied by 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 thick ascending limb of the loop of Henle and distal nephron may also contribute to the homeostatic natriuretic response to HS diet.

sodium chloride; kidney; natriuresis; salt-sensitive hypertension

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