ALTERED METABOLISM IN THE EXVIVO REMNANT KIDNEY .2. EFFECTS OF METABOLIC-INHIBITORS AND DIETARY-PROTEIN

To understand further the contribution of heightened net sodium reabso rption (T(Na+)) and other nontransport processes to increased and alte red metabolic activity of the rat remnant kidney (RK), isolated RK and normal kidneys (NK) were perfused with and without metabolic inhibito rs and following 4 weeks of low (12%)- or high (40%)-protein diet. 3-M ercaptopicolinate (200 muM) and 2-deoxyglucose (200 muM) reduced gluco se production and consumption, respectively, without altering oxygen c onsumption (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 inc reased glucose production in RK but not NK and reduced T(Na+) in NK bu t not RK. Dietary protein restriction reduced QO2 (2.18+/-0.29 vs. 4.1 3+/-0.20 mumol-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 ouaba in and alkalosis, but not other metabolic inhibitors, were quite disti nct in remnant versus normal kidneys, and (2) protein restriction limi ted sodium-transport-dependent and -independent hypermetabolism in RK.