Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10835195 | Nitric Oxide | 2005 | 8 Pages |
Abstract
We previously reported the stimulatory effect of endogenous nitric oxide (NO) on gastric acid secretion in the isolated mouse whole stomach and histamine release from gastric histamine-containing cells. In the present study, we investigated the effects of endogenous and exogenous NO on gastric acid secretion in urethane-anesthetized rats. Acid secretion was studied in gastric-cannulated rats stimulated with several secretagogues under urethane anesthesia. The acid secretory response to the muscarinic receptor agonist bethanechol (2 mg/kg, s.c.), the cholecystokinin2 receptor agonist pentagastrin (20 μg/kg, s.c.) or the centrally acting secretagogue 2-deoxy-d-glucose (200 mg/kg, i.v.) was dose-dependently inhibited by the NO synthase inhibitor NÏ-nitro-l-arginine (l-NNA, 10 or 50 mg/kg, i.v.). This inhibitory effect of l-NNA was reversed by a substrate of NO synthase, l-arginine (200 mg/kg, i.v.), but not by d-arginine. The histamine H2 receptor antagonist famotidine (1 mg/kg, i.v.) completely inhibited the acid secretory response to bethanechol, pentagastrin or 2-deoxy-d-glucose, showing that all of these secretagogues induced gastric acid secretion mainly through histamine release from gastric enterochromaffin-like cells (ECL cells). On the other hand, histamine (10 mg/kg, s.c.)-induced gastric acid secretion was not inhibited by pretreatment with l-NNA. The NO donor sodium nitroprusside (0.3-3 mg/kg, i.v.) also dose-dependently induced an increase in acid secretion. The sodium nitroprusside-induced gastric acid secretion was significantly inhibited by famotidine or by the soluble guanylate cyclase inhibitor methylene blue (50 mg/kg, i.v.). These results suggest that NO is involved in the gastric acid secretion mediated by histamine release from gastric ECL cells.
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Authors
Ko Hasebe, Syunji Horie, Tohru Noji, Kazuo Watanabe, Shingo Yano,