Role of purinergic system in tracheobronchial reactivity of healthy and bronchopathic subjects

We have investigated the effect of inhaled adenosine on bronchomotor tone in 16 healthy and 24 allergic and non-allergic bronchopathic subjects. We determined the inhaled adenosine dose-response curves after no treatment and after treatment with aminophylline (240 mg in 10 min), reproterol (90 mcg in 2 min) and salbutamol (100 mcg in 2 min) administered intravenously 15 min before adenosine and reproterol (500 mcg) and salbutamol (200 mcg) administered by inhalation from a metered aerosol 30 min before adenosine on separate days. Without prior treatment, inhaled adenosine caused bronchoconstriction in both groups of subjects (normal, and atopic and non-atopic asthmatic ones), but the peripheral airways revealed only a moderate change in normal subjects. Aminophylline caused a greater inhibition of adenosine bronchoconstriction than did reproterol. These results suggest that inhaled adenosine bronchoconstriction involved purinergic transmission and that it is mediated via a P1/Ri (A-1/R1) receptor. Aminophylline is a potent antagonist at purinoceptor level. Reproterol inhibits bronchoconstriction by a mechanism independent of its effect on beta-adrenergic receptors. Because salbutamol, i.e. a beta 2-agonist bronchodilator, did not inhibit adenosine-induced bronchoconstriction (or very nearly so), our results support the view that reproterol antagonizes P1/Ri (A1/R1) tracheobronchial receptors.