BRADYKININ AND MET-T-KININ-LEU STIMULATED PGE(2) PRODUCTION BY RAT MACROPHAGE AND FIBROBLAST

T-kininogen degradation and kinin release were observed in rat macroph ages cultured under acidic conditions. Bradykinin and Met-T-kinin-Leu (a kinin precursor) stimulated PGE(2) production by macrophages and fi broblasts but had no effect on O-2(-) production. PGE(2) production by macrophages stimulated with 10 mu M bradykinin increased by approxima tely 148% compared to non-stimulated macrophages (0.47 +/- 0.13 vs 0.3 1 +/- 0.16 ng 10(6) cells(-1) 30 min(-1)), and increased by 161% in st imulated as opposed to non-stimulated fibroblasts (0.50 +/- 0.07 vs 0. 31 +/- 0.05 ng 10(5) cells(-1) 30 min(-1)). No O-2(-) production was d etectable in fibroblasts despite stimulation with PMA, A23187, bradyki nin, and Met-T-kinin-Leu. O-2(-) production by macrophages was 4.2 +/- 0.3 and 3.0 +/- 0.2 nmol 10(6) cells(-1) min(-1) after stimulation wi th PMA and A23187, respectively, but no O-2(-) production was observed after stimulation with bradykinin or Met-T-kinin-Leu. These data sugg est that bradykinin and the kinin precursor are implicated in granulom atous tissue formation and wound healing through arachidonic acid and its metabolites but not through O-2(-).