Abstract
The nonadrenergic noncholinergic (NANC) relaxations in response to electrical stimulation and acetylcholine in the canine terminal ileum and ileocolonic junction were further characterized and the possible involvement of the putative NANC neurotransmitter ATP was investigated. During a norepinephrine-induced contraction, noncumulative administration of ATP and the nicotinic agonist, 1,1-dimethyl-4-phenylpiperazinium (DMPP) induced concentration-dependent relaxations in both the terminal ileum and ileocolonic junction; these responses were not inhibited by atropine, timolol or guanethidine. Desensitization to ATP blocked the ATP-induced relaxations, but not those to electrical stimulation or acetylcholine. All relaxations were abolished by tetrodotoxin. Theophylline or dipyridamole had no effect. Hexamethonium and desensitization to DMPP blocked the relaxations to acetylcholine and DMPP, but not those to electrical stimulation or ATP. The relaxations to acetylcholine, ATP and DMPP were inhibited by lidocaine. Thus, in the canine terminal ileum and ileocolonic junction, ATP induces NANC relaxations of neuronal origin, but ATP is unlikely to be the final NANC neurotransmitter mediating the relaxations to electrical stimulation or acetylcholine. These data also extend our previous observations on the presence of an inhibitory nicotinic innervation in these tissues.
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Evidence against ATP being the inhibitory transmitter released by nonadrenergic noncholinergic nerves in the canine ileocolonic junction.
