Stimulation of cholinergic nerves in dog intestine by adenine nucleotides

ATP, ADP, adenosine and AMP, but not adenine, inosine, or GMP, caused dose-related intestinal contractions when injected as intra-arterial bolus doses in vascularly perfused isolated segments of dog small bowel. The stimulatory effects of these agents were decreased by receptor densitization during exposure to high concentrations of ATP. ATP-induced contractions were also decreased by tetrodotoxin or atropine and after depletion of neuroinal acetylcholine content by hemicholinium. Depolarizing doses of nicotine blocked responses to ATP, but nicotinic receptor blockade with tetraethylammonium did not. It is concluded that ATP stimulates dog intestine by release of endogenous acetylcholine from intramural neural elements as a result of actions upon non-nicotinic receptors.