To investigate the effects of ischemia on renal metabolites, sequential slices of renal cortex were removed during 5 min of renal artery occlusion and for 5 min after release of occlusion. ATP concentrations rapidly fell during ischemia and rose during the post-ischemic period. Based on the rate of decline of ATP concentrations, the rate of ATP production was estimated to be 0.5 µ mol ATP/g/min. This is considerably less than the rate of ATP production estimated from renal O₂ consumption. During ischemia, AMP concentrations rose, confirming the activity of adenylate kinase. The control lactate/pyruvate ratio suggested that dog kidney cytosol is more reduced than the cytosol of rat liver and kidney. During ischemia, the lactate concentrations and the lactate/pyruvate ratio of dog renal cortex increased as expected, and fell after restoration of blood flow. β-Hydroxybutyrate concentrations were considerably lower than those previously reported for rat liver and kidney. The β-hydroxybutyrate/acetoacetate ratio was not measurable during ischemia. However, the mitochondrial redox state, calculated from the glutamate/α-ketoglutarate·NH⁺₄ ratio, was similar to previous reports and this ratio appropriately changed during the ischemic and post-ischemic period.