1 The influence of the nitric oxide (NO) biosynthesis inhibitor N0-nitro-L-arginine methyl ester (L-NAME) on the gastric relaxation induced by peripheral vagal stimulation was investigated in the anaesthetized rat.2 Peripheral vagal stimulation (10 Hz, 10 V, 1 ms for 20 s) induced a reproducible biphasic response: a short-lasting increase followed by a more pronounced decrease in intragastric pressure. This response also occurred in reserpinized animals (5mg kg-, i.p., 24 h before the experiment) while atropine (1 mg kg1, i.v.) abolished the initial increase in intragastric pressure. 3 L-NAME (1-30mg kg-',i.v.) induced an increase in arterial blood pressure. L-NAME (1 mg kg-i.v.) had no influence on the vagally induced gastric response while L-NAME (10 and 30mgkg-' i.v.) significantly changed it: the initial increase in intragastric pressure was enhanced while the decrease in intragastric pressure was reduced or abolished. N0-nitro-L-arginine (L-NNA, l0 mg kg-%, i.v.) had the same effect.4 An i.v. infusion of phenylephrine (10pgkg-lmin-1) inducing a pressor response similar to that produced by L-NAME (30mgkg-1, i.v.) did not influence the vagal gastric response. Infusion of L-arginine (300mgkg-' bolus, then lOOmgkg-lh-') starting 30min beforehand, reduced the pressor effect and prevented the influence of L-NAME (lOmgkg-, i.v.) on the vagal gastric response. After injection of both atropine (lmgkg-', i.v.) and L-NAME (30mgkg-', i.v.), the vagally induced decrease in intragastric pressure was similar to that obtained under control conditions. 5 These results are consistent with NO being released and inducing gastric relaxation during peripheral vagal stimulation. In addition to NO, another inhibitory non-adrenergic non-cholinergic neurotransmitter is released.