Adenosine-induced bronchoconstriction and its inhibition by nedocromil sodium.

The inhalation of adenosine or adenosine-5'-monophosphate (AMP) causes a reproducible and transient bronchoconstriction in both atopic and nonatopic asthmatic subjects that is not followed by a late-phase response. The response may be prevented by prophylactic treatment with histamine H1-receptor antagonist, local anesthetics, and atropine, which suggests that both mast cell mediator release and neuronal reflexes are involved. Adenosine- and AMP-induced bronchoconstriction are both blocked by cromolyn sodium and nedocromil sodium, with the PD20FEV1 for the latter approximately four times lower than that of cromolyn sodium in atopic asthmatic patients and approximately 2.3 times lower than that of cromolyn sodium in nonatopic asthmatic patients. We suggest that AMP-induced bronchoconstriction, in combination with other indirect-acting provicants, may be used to determine the effectiveness and mechanism of action of antiasthmatic drugs.