Recently, there has been an increasing interest in adenosine as a potential mediator of allergIc asthma. In the present study, we used the allergic rabbit model developed in our laboratory to study the airway responses to adenosine and receptor binding in allergic lung vs. normal. Neonatal, pathogen-free rabbit litter mates were injected intraperitoneally within 24 hr of birth with ragweed pollen extract(1 mg/mI) to produce preferentially aller-gen-specffic immunoglobulin E. Immunizaon produced bronchial airway hyperresponsiveness. Aerosolized adenosine(0.156-10 mg/me caused a dose-dependent bronchoconsthcon(PC adenosine= 1. 64±0.84 mg/mI). 9-Chloro-2-(2-furyl)[1, 2, 4] triazole [1, 5-c] qulnazolin-5-amine(CGS-1 5943), a nonxanthine adenosine receptor antagonist, significantly inhibited the adeno-sine-induced airway obstruction In term of dynamic compliance (P<. 05). Adenosine also increased the lung resistance in a dose-dependent manner which was significantly inhibited by CGS-15943(P<. 05). Nonlmmunized, pathogen-free, age-matched rabbfts (control) did not respond to adenosine at these same concentrations. Adenosine also produced a concentrationdependent(10-10 M) contraction of isolated tracheal and bronchial airway rings in vitro from allergic rabbits but had no detectable effect on normal rabbit airway smooth muscle. Penpheral aIrway smooth musdes(secondary and tertiary) were more responsive to adenosine than central (tracheal) airways. The contraction produced by 10 M adenosine in primary, secondary and tertiary airways was 90, 135 and 265% of the contraction produced by 50 mM KCI, respectively. CGS-15943