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), 0.28M NH₄Cl, or 0.28M KCl solutions in a pair-feeding protocol for five days (5d). Metabolic acidosis developed within 24h in NH₄Cl-, but not in KCl-loaded rats. Interestingly, NH₄Cl- but not KCl-loaded rats exhibited a significant natriuresis after 24h of treatment. Urinary Na⁺ excretion increased from 1.94 to 2.97 mEq/24h, P<0.001, and returned to below baseline level (1.67 mEq/l) after 5d of CMA. The protein abundance of cortical Na-Cl cotransporter (NCC) remained unchanged at 24h, but increased significantly (P<0.01) after 5d of CMA. The protein abundance of alpha-, beta-, and gamma-subunits of ENaC in the cortex decreased sharply during the first 24h, and then returned to baseline levels after 5d of CMA. Interestingly, Sgk1 expression decreased after 24h (-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 anti-natriuretic phase of metabolic acidosis. This adaptation prevents Na⁺ wasting and volume depletion during chronic acid insult.