AIM:Stress induces gastric ulceration in human andexperimental animals.People tend to smoke more cigaretteswhen under stress.Nitric oxide(NO)and nicotine haveopposing effects on gastric integrity.The present studyexamined the possible therapeutic benefit of NO in nicotine-treated rats with stress-induced gastric ulceration.METHODS:Rats drank a nicotine solution while control ratsdrank tap water for 20 days.The alkoloid was then replacedby water with or without supplementation of isosorbidedinitrate(NO donor)for an additional 10 days.Isosorbidedinitrate was given twice shortly before experiments(acute)or three times daily by oral garages for 10 days after the ratsstopped drinking nicotine solution.At the end of experiments,ulcer index,gastric adhesion mucus content and MPO activitywere measured and analysed.RESULTS:Nicotine treatment decreased gastric mucuscontent and intensified stress-induced gastric ulcer.A higherulcer index persisted even after the rats stopped drinkingnicotine solution for 10 days.Acute NO donor showed nobenefit on both mucus and ulcer index in nicotine treatmentor/and stress condition.Chronic NO donor treatment reversedthe worsening action of nicotine in stomach.Stress increasedgastric mucosal myeloperoxidase(MPO)activity,which wasantagonized by chronic NO treatment.However,nicotinewas unlikely to change mucosal MPO activity.CONCLUSION:The intensifying action of nicotine on stress-induced gastric ulceration persists for 10 days after cessation.Nicotine treatment significantly decreases gastric mucuscontent that can be restored by chronic NO donor treatment.The present study suggests that NO antagonizes theulcerogenic action of nicotine through a cytoprotective way. AIM: Stress induces gastric ulceration in human andexperimental animals.People tend to smoke more cigarettes under stress. Nitric oxide (NO) and nicotine haveopposing effects on gastric integrity. The present studyexamined the possible therapeutic benefit of NO in nicotine-treated rats with stress- induced gastric ulceration. METHODS: Rats drank a nicotine solution while controlling ratsdrank tap water for 20 days. The alkoloid was then replaced by water with or without supplementation of isosorbided initrate (NO donor) for an additional 10 days. Isosorbided initrate was given twice short before before experiments ( acute) or three times daily by oral garages for 10 days after the rats staged drinking nicotine solution. At the end of experiments, ulcer index, gastric adhesion mucus content and MPO activity we measured and analyzed .RESULTS: Nicotine treatment decreased gastric mucus content and intensified stress- induced gastric ulcer. A higher ulcer index persisted even after the rats stopped drinking nicotine solu tion for 10 days. Acute NO donor showed nobenefit on both mucus and ulcer index in nicotine treatmentor / and stress condition. Chronic NO donor of the switched on worsening action of nicotine in stomach. Stressed increased gastric mucosal myeloperoxidase (MPO) activity, which wasantagonized by chronic NO treatment. Although, nicotine was unlikely to change mucosal MPO activity. CONCLUSION: The intensifying action of nicotine on stress-induced gastric ulceration persists for 10 days after cessation. Nototin treatment is significantly reduced by gastric mucuscontent that can be restored by chronic NO donor treatment. present study suggests that NO antagonizes the ulcerogenic action of nicotine through a cytoprotective way.