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Metabolic acidosis has dual effects on sodium handling by rat kidney

Departments of ¹Internal Medicine and ²Surgery, University of Cincinnati Medical Center, Cincinnati, Ohio

Submitted 19 August 2005 ; accepted in final form 16 February 2006

Chronic metabolic acidosis (CMA) is associated with decreased NaCl reabsorption in the proximal tubule (PT). However, the effect of CMA on Na⁺ transport in the distal tubule (DT) and collecting duct (CD) is poorly understood. Rats were placed in metabolic cages and had access to water (control), 0.28 M NH₄Cl, or 0.28 M KCl solutions in a pair-feeding protocol for 5 days (5d). Metabolic acidosis developed within 24 h in NH₄Cl-, but not in KCl-loaded rats. Interestingly, NH₄Cl- but not KCl-loaded rats exhibited a significant natriuresis after 24 h of treatment. Urinary Na⁺ excretion increased from 1.94 to 2.97 meq/24 h (P < 0.001) and returned to below baseline level (1.67 meq/l) after 5d of CMA. The protein abundance of the cortical Na-Cl cotransporter (NCC) remained unchanged at 24 h, but increased significantly (P < 0.01) after 5d of CMA. The protein abundance of -, -, and -subunits of the epithelial Na⁺ channel (ENaC) in the cortex decreased sharply during the first 24 h and then returned to baseline levels after 5d of CMA. Interestingly, Sgk1 expression decreased after 24 h (–31%, P < 0.05) and then returned to baseline after 5d of CMA. Nedd4–2 expression was not altered during CMA. CMA enhanced serum aldosterone levels by 54% and increased the expression of aldosterone synthase in the adrenal gland by 134% after 5d of CMA. In conclusion, metabolic acidosis has dual effects on urinary Na⁺ excretion. The early natriuresis results from decreased Na⁺ reabsorption in the PT and Sgk1-related decreased ENaC activity in the DT and CD. Aldosterone-induced upregulation of NCC, Sgk1, and ENaC likely contributes to the antinatriuretic phase of metabolic acidosis. This adaptation prevents Na⁺ wasting and volume depletion during chronic acid insult.

natriuresis; aldosterone; distal tubule; epithelial Na⁺ channel; Sgk1

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