Influence of NG‐nitro‐l‐arginine methyl ester on vagally induced gastric relaxation in the anaesthetized rat

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Abstract
1 . The influence of the nitric oxide (NO) biosynthesis inhibitor NG-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 (5 mg kg−1, i.p., 24 h before the experiment) while atropine (1 mg kg−1, i.v.) abolished the initial increase in intragastric pressure. 3 . l-NAME (1–30 mg kg−1, i.v.) induced an increase in arterial blood pressure. l-NAME (1 mg kg−1, i.v.) had no influence on the vagally induced gastric response while l-NAME (10 and 30 mg kg−1 i.v.) significantly changed it: the initial increase in intragastric pressure was enhanced while the decrease in intragastric pressure was reduced or abolished. NG-nitro-l-arginine (l-NNA, 10 mg kg−1, i.v.) had the same effect. 4 . An i.v. infusion of phenylephrine (10 μg kg−1 min−1) inducing a pressor response similar to that produced by l-NAME (30 mg kg−1, i.v.) did not influence the vagal gastric response. Infusion of l-arginine (300 mg kg−1 bolus, then 100 mg kg−1 h−1) starting 30 min beforehand, reduced the pressor effect and prevented the influence of l-NAME (10 mg kg−1, i.v.) on the vagal gastric response. After injection of both atropine (1 mg kg−1, i.v.) and l-NAME (30 mg kg−1, 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.