Acid–base status is considered the major factor controlling renal production from glutamine, with maximal values found in chronic acidosis. However, metabolic inhibitors have been shown to increase production without acid–base change; the mechanism for this increase is unclear. Fluorocitrate was administered to dogs with chronic metabolic alkalosis. Following fluorocitrate total renal production rose from 32 ± 5 to 104 ± 15 μmol/(min∙100 mL glomerular filtration rate (GFR)) (p < 0.01) and glutamine extraction rose from 26 ± 8 to 65 ± 8 μmol/(min∙100 mL GFR) (p < 0.01). These values approximate maximal values found in chronic acidosis. Lactate utilization fell from 165 ± 19 to 99 ± 7 μmol/(min∙100 mL GFR) following fluorocitrate (p < 0.01). Citrate extraction fell to zero and alanine production rose from 27 ± 4 to 46 ± 7 μmol/(min∙100 mL GFR) (p < 0.01). Oxygen consumption remained unchanged following fluorocitrate, 584 ± 29 vs. 549 ± 29 μmol/(min∙100 mL GFR). These results demonstrate that in the presence of metabolic inhibition in the kidney, ATP production remains constant. This is achieved by increased utilization of one substrate, glutamine, when the ATP production from other substrates is reduced. Thus the necessity to maintain constant ATP production appears to modulate renal production.Key words: ammonium production, metabolic inhibitors, oxygen uptake.