Recent work has suggested that adenosine may be involved in asthma via the activation of A₁ receptors. However, the role of the recently cloned A₃ receptor in airways is largely unknown. In the present study, we have investigated the role of the A₃ receptor in adenosine‐induced bronchoconstriction in allergic rabbits.

Aerosol challenge of antigen (Ag) immunized rabbits with the adenosine precursor, adenosine 5′‐monophosphate (AMP), resulted in a dose‐dependent fall in dynamic compliance (C_dyn). The maximum fall in C_dyn in these rabbits was significantly greater than that in litter matched, sham immunized animals (P < 0.05). However, there was no significant difference in the maximum increase in airways resistance (R_L) between Ag and sham immunized rabbits (P > 0.05).

Aerosol challenge of Ag immunized rabbits with cyclopentyl‐adenosine (CPA) (A₁‐receptor agonist) elicited a dose‐dependent fall in C_dyn in Ag immunized rabbits and the maximum fall in C_dyn in these rabbits was significantly greater than that observed in sham immunized rabbits (P < 0.05). Similarly, CPA induced dose‐dependent increases in R_L in Ag immunized rabbits whereas sham immunized rabbits failed to respond to CPA within the same dose range. The maximum increase in R_L in Ag immunized rabbits was significantly greater than that of sham immunized rabbits (P < 0.05).

Aerosol challenge of either Ag or sham immunized rabbits with the A₃ agonist aminophenylethy‐ladenosine (APNEA) did not elicit dose‐dependent changes in either R_L or C_dyn. Moreover, there was no significant difference in the maximum response, measured by either parameter, between the two animal groups (P > 0.05).

These data provide further evidence for a role of the A₁ receptor in the airways, but do not support a role for the A₃ receptor in adenosine‐induced bronchoconstriction in the allergic rabbit.