T-kininogen degradation and kinin release were observed in rat macrophages cultured under acidic conditions. Bradykinin and Met-T-kinin-Leu (a kinin precursor) stimulated PGE2 production by macrophages and fibroblasts but had no effect on O2- production. PGE2 production by macrophages stimulated with 10 microM bradykinin increased by approximately 148% compared to non-stimulated macrophages (0.47 +/- 0.13 vs 0.31 +/- 0.16 ng 10(6) cells-1 30 min-1), and increased by 161% in stimulated as opposed to non-stimulated fibroblasts (0.50 +/- 0.07 vs 0.31 +/- 0.05 ng 10(5) cells-1 30 min-1). No O2- production was detectable in fibroblasts despite stimulation with PMA, A23187, bradykinin, and Met-T-kinin-Leu. O2- production by macrophages was 4.2 +/- 0.3 and 3.0 +/- 0.2 nmol 10(6) cells-1 min-1 after stimulation with PMA and A23187, respectively, but no O2- production was observed after stimulation with bradykinin or Met-T-kinin-Leu. These data suggest that bradykinin and the kinin precursor are implicated in granulomatous tissue formation and wound healing through arachidonic acid and its metabolites but not through O2-.