[3H]bradykinin ([3H]BKN) was microinfused alone or in the presence of a 390 or 780 fold excess of BKN or angiotensin I (AI) into proximal tubules in Inactin anesthetized rats. Urinary excretion of 3H labeled material was measured, and intact peptide and its metabolites were identified and quantified. When [3H]BKN was administered with BKN or AI, urinary recovery of 3H labeled material was increased in a manner directly proportional to tubular length, suggesting that reabsorption of [3H]BKN is related to extent of tubular contact. BKN and AI were equally effective in inhibiting the reabsorption of [3H]BKN and its metabolites from proximal tubular fluid. In contrast, BKN but not AI effectively inhibited the enzymatic hydrolysis of [3H]BKN in the proximal tubule. The data suggest that the proximal tubular mechanism for reabsorbing BKN and its metabolites is of high capacity but not high specificity and that the mechanisms for enzymatic cleavage and reabsorption of BKN and its metabolites may have different specificities and capacities.