Acid secretion and nitric oxide synthase activity in gastric glands following hypoxia/reoxygenation and acidosis

Kim, H.; Kim,

Korean Journal of Pharmacology 31(1): 75-84


ISSN/ISBN: 0377-9459
Accession: 008096849

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Acid secretion and NO synthase activity were determined in isolated gastric glands following hypoxia/reoxygenation and acidosis to investigate the involvement of NO in acid secretion. Isolated gastric glands were exposed to hypoxia (30 min)/reoxygenation (1 h) and/or to acidosis (pH 6.0 and 4. 0). Acid secretion was measured by the ratio of (14C)-aminopyrine accumulation between intra- and extraglands. NO synthase activity was determined by percent conversion to (14C)-L-citrulline from (14C)-L-arginine, a precursor of NO. The results indicate that dibutyryl cAMP stimulated acid secretion dose-dependently but had no effect on NO synthase activity in basal gastric glands. Hypoxia/ reoxygenation significantly suppressed acid secretion both in unstimulated and stimulated gastric glands, which was exaggerated by acidosis. Constitutive NO synthase activity, not responded to dibutyryl cAMP, was also inhibited by hypoxia/reoxygenation and acidosis. In conclusion, pathologic state of gastric mucosa such as hypoxia/reoxygenation and acidosis suppresses both acid secretion and NO release but the role of NO in acid secretion stimulated by dibutyryl cAMP in basal gastric glands is not significant.