Effects of K+-deficient diets with and without NaCl supplementation on Na+, K+, and H2O transporters' abundance along the nephron

MTX Nguyen, LE Yang, NK Fletcher… - American Journal …, 2012 - journals.physiology.org
MTX Nguyen, LE Yang, NK Fletcher, DH Lee, H Kocinsky, S Bachmann, E Delpire
American Journal of Physiology-Renal Physiology, 2012journals.physiology.org
Dietary potassium (K+) restriction and hypokalemia have been reported to change the
abundance of most renal Na+ and K+ transporters and aquaporin-2 isoform, but results have
not been consistent. The aim of this study was to reexamine Na+, K+ and H2O transporters'
pool size regulation in response to removing K+ from a diet containing 0.74% NaCl, as well
as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet
electrolytes. Sprague-Dawley rats (n= 5–6) were fed for 6 days with one of these diets: 2 …
Dietary potassium (K+) restriction and hypokalemia have been reported to change the abundance of most renal Na+ and K+ transporters and aquaporin-2 isoform, but results have not been consistent. The aim of this study was to reexamine Na+, K+ and H2O transporters' pool size regulation in response to removing K+ from a diet containing 0.74% NaCl, as well as from a diet containing 2% NaCl (as found in American diets) to blunt reducing total diet electrolytes. Sprague-Dawley rats (n = 5–6) were fed for 6 days with one of these diets: 2% KCl, 0.74% NaCl (2K1Na, control chow) compared with 0.03% KCl, 0.74% NaCl (0K1Na); or 2% KCl, 2%NaCl (2K2Na) compared with 0.03% KCl, 2% NaCl (0K2Na, Na+ replete). In both 0K1Na and 0K2Na there were significant decreases in: 1) plasma [K+] (<2.5 mM); 2) urinary K+ excretion (<5% of control); 3) urine osmolality and plasma [aldosterone], as well as 4) an increase in urine volume and medullary hypertrophy. The 0K2Na group had the lowest [aldosterone] (172.0 ± 17.4 pg/ml) and lower blood pressure (93.2 ± 4.9 vs. 112.0 ± 3.1 mmHg in 2K2Na). Transporter pool size regulation was determined by quantitative immunoblotting of renal cortex and medulla homogenates. The only differences measured in both 0K1Na and 0K2Na groups were a 20–30% decrease in cortical β-ENaC, 30–40% increases in kidney-specific Ste20/SPS1-related proline/alanine-rich kinase, and a 40% increase in medullary sodium pump abundance. The following proteins were not significantly changed in both the 0 K groups: Na+/H+ exchanger isoform 3; Na+-K+-Cl cotransporter; Na+-Cl cotransporter, oxidative stress response kinase-1; renal outer medullary K+ channel; autosomal recessive hypercholesterolemia; c-Src, aquaporin 2 isoform; or renin. Thus, despite profound hypokalemia and renal K+ conservation, we did not confirm many of the changes that were previously reported. We predict that changes in transporter distribution and activity are likely more important for conserving K+ than changes in total abundance.
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