RÉSUMÉ
The role of NO in the regulation of gastric acid secretion was examined in the anaesthetized adult male albino rats. Continuous i.v. infusion of the NO donor, sodium nitroprusside [SNP, 12mg/kg/h] significantly inhibited both basal and stimulated gastric acid secretion which was mediated neuronally by gastric distension [20 cm H2O or i.v. bolus administration of 2-deosxy -D- glucose [150 mg/kg], as well as gastric acid responses induced by i.v infusion of submaximal doses of pentagastrin [8 micro g/kg/h]. By contrast, gastric acid responses to i.v. infusion of submaximal doses of histamine [1 mg/kg/h] were not influenced by the NO donor. Pretreatment with N[G] - nitro-L-arginine methylester[L-NAME, 10mg/kg, i.v.] did not affect basal acid secretion, but significantly potentiated the increase in acid secretion induced by 2-deoxy-D- glucose which was almost completely antagonized by coadministration of L-arginine [500 mg/kg, i.p.] and slightly augmented the acid secretory response to pentagastrin. Moreover, it was found that pentagastrin infusion caused an increase in luminal release of histamine and this response was significantly suppressed by i.v infusion of the NO donor.Intraperitoneal [i.p] administration of cimetidine [60 mg/kg], a histamine H2-receptor antagonist, significantly inhibited the increase in acid secretion in response to 2-deoxy-D-glucose [150 mg/kg, i.v.], pentagastrin [8 micro g/kg/h, i.v] and histamine [I mg/kg/h, i.v.] infusion. In conclusion, the present study suggests that NO has an inhibitory action on gastric acid secretion that may be through suppression of histamine release from enterochromaffin like [ECL] cells