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

Abstract

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 H(2)O 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.

• Authors: Mien T X Nguyen, Li E Yang, Nicholas K Fletcher, Donna H Lee, Hetal Kocinsky, Sebastian Bachmann, Eric Delpire, Alicia A McDonough
• Journal: American journal of physiology. Renal physiology (Am J Physiol Renal Physiol) Vol. 303 Issue 1 Pg. F92-104 (Jul 01 2012) ISSN: 1522-1466 [Electronic] United States
• PMID: 22496411 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)

Chemical References

• Epithelial Sodium Channels
• Potassium, Dietary
• Sodium Chloride, Dietary
• Sodium-Hydrogen Exchangers
• Sodium-Potassium-Chloride Symporters

Topics

• Animals
• Epithelial Sodium Channels (metabolism)
• Male
• Nephrons (drug effects, metabolism)
• Phosphorylation (drug effects)
• Potassium Deficiency (metabolism)
• Potassium, Dietary (pharmacology)
• Rats
• Rats, Sprague-Dawley
• Sodium Chloride, Dietary (pharmacology)
• Sodium-Hydrogen Exchangers (metabolism)
• Sodium-Potassium-Chloride Symporters (metabolism)