Cyclic Amp and the release of antral gastrin.
The isolated, vagally innervated antral pouches in anesthetized dogs were irrigated with 095% acetylcholine chloride (Ach) or a 0.4 M mixture of non-essential amino acids (AA), or distended at 30 cm H2O pressure. In addition,2-deoxy-D-glucose (2-DG) was administered intravenously. Significant increases in antral venous gastrin, caused by gastrin releasers, were associated with a significant rise in cAMP content in the antral mucosa. Acidification of the antrum with simultaneous administration of 2-DG, and acidified AA abolished gastrin release, and significantly reduced mucosal cAMP. Acidified Ach and distension of the antrum with 0.1 N HC1 supressed gastrin levels without significantly changing the mucosal cAMP content. Since the augmented gastrin release was accompanied by an increased mucosal cAMP, the results suggest that cAMP participates in the action of gastrin secretagogues.
D000109:Acetylcholine / Q000494:pharmacology; D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D000242:Cyclic AMP / Q000502:physiology*; D003847:Deoxyglucose / Q000494:pharmacology; D004285:Dogs; D005753:Gastric Mucosa / Q000378:metabolism*; D005755:Gastrins / Q000097:blood / Q000378:metabolism*; D011706:Pyloric Antrum / Q000378:metabolism*; D014630:Vagus Nerve / Q000502:physiology
D000596:Amino Acids; D005755:Gastrins; D003847:Deoxyglucose; D000242:Cyclic AMP; D000109:Acetylcholine