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Adenosine‐modulation of cholinergic and non‐adrenergic non‐cholinergic neurotransmission in the rabbit iris sphincter

1 The characteristics of smooth muscle responses to transmural nerve stimulation in the rabbit iris sphincter were examined. 2 Transmural stimulation elicited a composite contractile response that could be divided in two phases. Atropine abolished the phase I contraction and inhibited the phase II contraction. The atropine‐resistant component of the phase II contraction which was unaltered by sympathetic denervation, was mimicked by substance P and abolished by capsaicin. 3 Adenosine inhibited the phase I contraction. The adenosine analogue L‐N6‐phenylisopropyladenosine (L‐PIA) was more potent than 5′‐N‐ethylcarboxamideadenosine (NECA) in mimicking this adenosine effect. 4 By contrast, adenosine enhanced the phase II contraction in non‐pretreated preparations, as well as the atropine‐resistant capsaicin‐sensitive part of this contraction. Here, NECA was more potent than L‐PIA. 5 Adenosine, NECA, L‐PIA and D‐PIA also enhanced the atropine‐sensitive component of the phase II contraction, as well as the contractile response to exogenous acetylcholine or carbachol, but not to exogenous substance P. In this respect, L‐PIA was the most powerful adenosine analogue with at least 10 fold higher potency than D‐PIA. 6 The adenosine antagonist 8‐p‐sulphophenyltheophylline enhanced the phase I contraction and decreased the capsaicin‐sensitive non‐adrenergic non‐cholinergic component of the phase II contraction. 7 We conclude that adenosine inhibited the nerve‐induced cholinergic twitch (phase I) responses by action at prejunctional A1‐receptors. Furthermore, adenosine enhanced the phase II contractile responses via postjunctional enhancement of the cholinergic transmission by action at A1‐receptors, and via enhancement of the non‐adrenergic non‐cholinergic transmission by action at presumably prejunctional A2 receptors.