To examine whether furosemide affects the plasma concentration and urinary excretion of purine bases, adenosine, and uridine, we administered 20 mg furosemide intravenously to 6 healthy subjects. Furosemide decreased the plasma concentration of hypoxanthine by 39% and increased plasma renin activity (PRA) and the plasma concentration of protein by 3.4-fold and 9%, respectively, at 90 minutes after administration. Furthermore, it decreased the urinary excretion of hypoxanthine, xanthine, and uric acid by 47%, 49%, and 49%, respectively, and the fractional clearance of xanthine and uric acid by 44% and 47%, respectively, during the 1-hour period between 60 and 120 minutes after administration. However, furosemide did not affect the plasma concentration or urinary excretion of adenosine and uridine. In addition, in an in vitro incubation study of erythrocytes, furosemide (10 microg/mL) did not affect the concentration of hypoxanthine in the incubation medium or the activity of erythrocyte purine nucleoside phosphorylase and 5'-nucleotidase. These results imply that xanthine may share a renal transport pathway with uric acid. Further, it is suggested that the furosemide-induced decrease in hypoxanthine may be ascribable to a decrease in adenosine triphosphate (ATP) degradation related to the inhibition of chloride transport in the body.