Abstract In the present study, the effect of bradykinin on basal and precontracted mouse-isolated trachea was investigated. In basal conditions mouse-isolated tracheal rings do not respond to bradykinin. However, when the tracheal rings were precontracted with carbachol (107M) a relaxation with bradykinin (31093107) was found. The maximal response amounted 69.74.1% (n=15) with a pD2 value of 7.20.21. The selective bradykinin B2 receptor antagonist HOE 140 (1010108M) antagonized the bradykinin-induced relaxation, while the bradykinin B1 receptor antagonist des-Arg9-Leu8-bradykinin (106M) had no influence. The selective bradykinin B1 receptor agonist des-Arg9-bradykinin (106M) caused a small relaxation (8.42.5%, n=6), which could be antagonized completely by the selective bradykinin B1 receptor antagonist des-Arg9-Leu8-bradykinin (106M) while addition of the selective bradykinin B2 receptor antagonist HOE 140 (108M) was without effect. In the presence of indomethacin (106M) the relaxation of bradykinin was completely abolished. Pretreatment of the tracheal rings with capsaicin, or the presence of the selective NK1 receptor antagonist RP 67851 (106M) or the presence of the nitric oxide synthase inhibitor L-NAME (3104M) had no effect on the bradykinin-induced relaxation. In conclusion, these results demonstrate that the mouse-isolated tracheal is a preparation in which bradykinin exerts a relaxant response via stimulation of bradykinin B2 receptors. This response is probably mediated by prostaglandines.