To understand further the contribution of heightened net sodium reabsorption (T_Na+) and other nontransport processes to increased and altered metabolic activity of the rat remnant kidney (RK), isolated RK and normal kidneys (NK) were perfused with and without metabolic inhibitors and following 4 weeks of low (12%)- or high (40%)-protein diet. 3-Mercaptopicolinate (200 μM) and 2-deoxyglucose (200 μM) reduced glucose production and consumption, respectively, without altering oxygen consumption (QO₂). Ouabain reduced T_Na+ and QO₂ in NK but not RK, and increased glucose consumption in RK (by 67%, p < 0.02, n = 12) and NK (by 54%, p < 0.05, n = 12). Raising perfusate pH by 0.3 U to 7.65 increased glucose production in RK but not NK and reduced T_Na+ in NK but not RK Dietary protein restriction reduced QO₂ (2.18 ± 0.29 vs. 4.13 ± 0.20 μmol^-1 min^-1 g^-1 p < 0.001), T_Na+ (8.74 ± 4.39 vs. 38.83 ± 8.32, p < 0.01) and ammoniagenesis (0-30 min, 0.16 ± 0.05 vs. 0.32 ± 0.10, p < 0.05) in RK, but not NK. In summary: (1) responses to ouabain and alkalosis, but not other metabolic inhibitors, were quite distinct in remnant versus normal kidneys, and (2) protein restriction limited sodium-transport-dependent and -independent hypermetabolism in RK.

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