We previously demonstrated that the bradykinin-induced contraction of human isolated small bronchi is inhibited by indomethacin, capsaicin ( N-methyl- N-6-nonenamide) and ruthenium red but not by tachykinin receptor antagonists. The thromboxane A 2 receptor (TP receptor) antagonist GR32191 ((1 R-(1α( Z),2β,3β,5α))-(+)-7-(5-(((1,1′-biphenyl)-4-yl)-methoxy)-3-hydroxy-2-(1-piperidinyl)cyclopentyl)-4-heptenoic acid, hydrochloride) (10 −10 to 10 −8 M) dose dependently inhibited the effect of bradykinin, suggesting the mediation of the TP receptor in the action of bradykinin. With higher concentrations of GR32191 (10 −7 and 10 −6 M) bradykinin induced a relaxation which was inhibited by indomethacin and by the bradykinin B 2 receptor antagonist Hoe 140 ( d-Arg 0[Hyp 3,Thi 5, d-Tic 7,Oic 8]bradykinin). The thromboxane A 2 synthase inhibitor dazoxiben (4-(-2-(1 H-imidazol-1-yl)ethoxy) benzoic acid hydrochloride) 10 −6 M inhibited the bradykinin-induced contraction, suggesting that throm-boxane A 2 was involved in TP receptor stimulation. The thromboxane A 2 mimetic U-46619 (9,11-dideoxy-11α,9α-epoxy-methano-prostaglandin F 2α)-induced contraction of human distal bronchi was not inhibited by capsaicin and ruthenium red. Our data suggest that bradykinin contracts human isolated small bronchi through thromboxane A 2 release. The inhibitory effect of ruthenium red and capsaicin on the bradykinin response may be due to inhibition of thromboxane A 2 release or arachidonic mobilisation.