ATP-MgCl2 administration had been shown to accelerate the recovery of renal function following warm ischemia. However, since the major breakdown product of ATP is adenosine, the relative contribution of ATP vs. adenosine in improving renal function following ischemia remains to be determined. To study this, kidneys were subjected to 45 min of normothermic ischemia and then perfused at 100 mmHg with oxygenated Krebs-HCO3 buffer containing albumin, [3H]inulin, substrates, and either 0.3 mM ATP-MgCl2 or adenosine-MgCl2 for 110 min. Perfusate and time urine samples were collected and analyzed for radioactivity and [Na+]. The functional parameters indicated that although adenosine-MgCl2 treatment provided a transient improvement, it failed to provide a sustained improvement in renal function or attain control values compared with ATP-MgCl2 treatment. Thus, the salutary effects of ATP-MgCl2 following warm ischemia in the kidney are not mediated by adenosine.