Airway hyperreactivity (AHR) is an important characteristic feature of asthma. Recently, it has been recognized that airway inflammation underlies the phenomenon of AHR. Kinins such as bradykinin (BK) and kallidin (KD) have been implicated as mediators of airway inflammatory diseases. Tachykinins such as substance P (SP) and neurokinin A (NKA) produce a variety of effects on the airways. These effects include changes in bronchomotor tone, vasodilatation, increase in vascular permeability and facilitation of the release of other transmitters. Non-cholinergic responses are due to release of neuropeptides such as tachykinins from sensory nerve endings. Kinins and tachykinins have been implicated in neurogenic inflammation. The O3 exposure (3 ppm, 30 min) induced AHR to ACh in guinea pigs. The O3-induced AHR was significantly enhanced by pretreatment with captopril, a kininase II inhibitor. Infusion of subthreshold dose of BK and KD developed AHR to ACh. The O3-induced AHR was significantly inhibited by pretreatment with capsaicin. Infusion of the subthreshold dose of SP and NKA developed an AHR to ACh. The KD-induced AHR was inhibited by pretreatment with capsaicin. Kinins and tachykinins may be therefore involved in the O3-induced AHR, and kinins may act through tachykinin intervention on the O3-induced AHR.