Experiments were performed to examine the possible interaction between the cholinergic transmitter and the reactivity of gastric arteries to adrenergic activation. Helical strips of dogs' gastric arteries were mounted for isometric tension recording. The strips contracted on exposure to norepinephrine; these contractions were inhibited by phenoxybenzamine. Electrical stimulation caused an increase in tension, which was abolished by tetrodotoxin and phenoxybenzamine, indicating that electrical stimulation causes contraction by liberation of norepinephrine. Acetylcholine did not alter basal tension; it caused relaxation during responses to electrical simulation, but not during those to norepinephrine. The relaxation caused by acetylcholine was abolished by atropine. This indicates that acetylcholine inhibits adrenergic neurotransmission in the dog's gastric artery. When added during electrical stimulation, atropine caused an increase in tension. The same concentrations of atropine did not affect basal tension or the response to norephrine. Physostigmine depressed the response to electrical stimulation, but not that to norepinephrine. In the blood-perfused stomach of the intact dog, vagal stimulation depressed vasoconstrictions caused by sympathetic nerve stimulation more than comparable constrictor responses obtained with the infusion of norepinephrine. These experiments suggest that liberated acetylcholine can modulate adrenergic neurotransmission in the gastric blood vessels. The removal of cholinergic inhibition on the release of norepinephrine may help explain why vagotomy has a beneficial effect on gastric bleeding.