Apparent enhancement of cholinergic transmission in rabbit bronchi via adenosine A2 receptors.

Adenosine and its derivatives enhanced the contractile responses to transmural nerve stimulation in rabbit isolated bronchial smooth muscle. 5'-N-Ethylcarboxamideadenosine (NECA) was the most potent adenosine analogue studied. Enhancement of contractile responses by NECA was competitively antagonized by 8-p-sulfophenyltheophylline. Guanethidine, mepyramine, capsaicin or eicosatetraynoic acid did not antagonize the enhancement elicited by adenosine or NECA. NECA did not enhance the contractile responses to exogenously applied acetylcholine or contractile responses elicited after administration of tetrodotoxin. We suggest that adenosine, via an action at A2 receptors, enhances contractile responses to nerve stimulation in rabbit bronchial muscle. Methylxanthines are competitive antagonists at these extracellular receptors. The enhancement probably involves a sodium-dependent mechanism but not adrenergic mechanisms or release of histamine, substance P or arachidonate metabolites. The enhancement indicates increased cholinergic transmitter release or action, but release of a secondary spasmogenic or decreased release of an inhibitor mediator cannot be excluded. The results may indicate a role for adenosine in asthma.