The pharmacological effects of 4,5-(2-(4-azido-2- nitroanilino)ethyl)imidazole (AAH) was evaluated in-vitro on guinea- pig aorta and dog trachealis. Aorta from male English-short-haired- guinea-pig and trachea from Mongrel-dogs were removed, mounted, and attached to transducers for measurements of isometric contractile responses. The tissues were incubated with AAH for 5 minutes; some of the samples were irradiated. Control tissues were irradiated in the absence of AAH. Photolyzed and non photolyzed tissues were exposed to increasing concentrations of histamine (51456), acetylcholine (51843) (AC), norepinephrine (51412) (NE), diphenylhydramine (58731), cimetidine (51481619) (CM) and potassium- chloride (PC) (7447407). AAH did not cause contraction when added to the organ bath, while photolyzed AAH caused 38 percent decrease in maximum response. Exposure of aorta to histamine following incubation with AAH and its subsequent removal from the tissues resulted in a non equilibrated competitive contractile response. Photolyzed AAH had no effect on aorta response to NE or PC. In trachealis it did not antagonize the contractile response to histamine, nor did it affect the responses to AC and PC in this organ. The possibility that this difference in response of aorta afd trachealis to photolyzed AAH may be caused by the lack of histamine receptors in trachealis was not substantiated, because the time when AAH was converted by photolysis from an equilibrated competitive antagonist to a non equilibrated competitive antagonist was the same for both tissues. Diphenylhydramine produced a 4.9 fold greater effect in aorta than trachealis, and CM potentiated contractile response of aorta to histamine but not of trachealis. Histamine did not relax either muscle system with induced tone, indicating that the resistance of trachealis to photolyzed AAH did not involve the inhibition of H2 receptors. The authors conclude that the difference in response of the two tissues to photolyzed AAH is due to the differences in the characteristics of the H1 receptors.