A study of beta-adrenergic and prostaglandin receptors in patients with aspirin-induced bronchospasm.

Nine patients with aspirin-induced bronchospasm were compared with age-matched normal controls to test the hypothesis that a defect in the beta-adrenergic system could lead to excessive dependence on prostaglandins to maintain bronchodilator function. Lymphocyte beta-receptor density and affinity were measured by 3H-dihydroalprenolol binding. Beta-receptor function was measured in terms of cyclic AMP accumulation in response to isoproterenol. Prostaglandin (PG) responsiveness was measured in terms of cyclic AMP accumulation caused by PGE1 stimulation. No difference was found in either ther number of beta-adrenergic receptors (1234 +115 vs 1213 +82) or dissociation constant (1.40 +0.23 nM vs 1.19 +0.07nM) (mean +SEM) between the asthmatic and the control group, respectively. Furthermore, neither group showed any difference in maximally stimulated cyclic AMP in response to isoproterenol and PGE 1. Thus we find no evidence of an inherent defect of beta-adrenergic receptor and function to account for the susceptibility to aspirin-induced bronchospasm.