Na⁺ loading without Cl⁻ fails to increase blood pressure in the DOCA model. We compared the changes in the total body (TB) effective Na⁺, K⁺, Cl⁻, and water (TBW) content as well as in intracellular (ICV) or extracellular (ECV) volume in rats receiving DOCA-NaCl, DOCA-NaHCO₃, or DOCA-KHCO₃. We divided 42 male rats into 5 groups. Group 1 was untreated, group 2 received 1% NaCl, and groups 3, 4, and 5 were treated with DOCA and received 1% NaCl, 1.44% NaHCO₃, or 1.7% KHCO₃ to drink. We measured mean arterial blood pressure (MAP) directly after 3 wk. Tissue electrolyte and water content was measured by chemical analysis. Compared with control rats, DOCA-NaCl increased MAP while DOCA-NaHCO₃ and DOCA-KHCO₃ did not. DOCA-NaCl increased TBNa⁺ 26% but only moderately increased TBW. DOCA-NaHCO₃ led to similar TBNa⁺ excess, while TBW and ICV, but not ECV, were increased more than in DOCA-NaCl rats. DOCA-KHCO₃ did not affect TBNa⁺ or volume. At a given TB(Na⁺+K⁺) and TBW, MAP in DOCA-NaCl rats was higher than in control, DOCA-NaHCO₃, and DOCA-KHCO₃ rats, indicating that hypertension in DOCA-NaCl rats was not dependent on TB(Na⁺+K⁺) and water mass balance. Skin volume retention was hypertonic compared with serum and paralleled hypertension in DOCA-NaCl rats. These rats had higher TB(Na⁺+K⁺)-to-TBW ratio in accumulated fluid than DOCA-NaHCO₃ rats. DOCA-NaCl rats also had increased intracellular Cl⁻ concentrations in skeletal muscle. We conclude that excessive cellular electrolyte redistribution and/or intracellular Na⁺ or Cl⁻ accumulation may play an important role in the pathogenesis of salt-sensitive hypertension.