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

Abstract

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.

Effect of pancreatic polypeptide on gastric accommodation and gastric emptying in conscious rats

“…Indeed, Lefebvre et al showed that L-NAME reduced IGP decrease during vagal nerve stimulation in anesthetized rats, indicating that NO release is crucial for this response (21). Another group showed that spontaneous antral relaxations were abolished by L-NAME (12).…”

Nitrergic contribution to gastric relaxation induced by glucagon-like peptide-1 (GLP-1) in healthy adults

“…Postprandial accommodation is primarily attributed to nutrient-driven stimulation of vagal activity, which activates enteric nitrergic pathways to relax the stomach (9,23,27,43). Thus L-NMMA blunted postprandial accommodation in healthy subjects (26,42).…”

“…However, how GLP-1 increases gastric volumes is not understood. Since vagally mediated nitric oxide (NO) release is partly responsible for gastric accommodation (9,23,27,43), vagal inhibition would be anticipated to reduce (not increase) fasting gastric volume and postprandial accommodation. There is increasing evidence to suggest that several effects of GLP-1 [e.g., inhibition of small bowel motility (33,46) and relaxation of pulmonary arterial smooth muscle in rats (14,37)] are mediated by NO.…”

Effects of brain stem cholecystokinin-8s on gastric tone and esophageal-gastric reflex

“…72). Much of the vagal NANC inhibitory effect on the stomach is mediated by the release of nitric oxide onto gastric smooth muscle (1,10,24,37,41,44,45,68). Perfusion with CCK-8s induces an excitation in most neurons, including identified gastrointestinal-projecting DMV neurons (4,7,13,23,38,47,48,65,66,75,79).…”