Mechanisms of insulin-induced relaxation of the canine proximal stomach after proximal gastric vagotomy

The aim of this study was to determine whether insulin-induced relaxation of the proximal stomach after proximal gastric vagotomy is mediated by vagal release of antral gastrin. In six conscious, fasted dogs following proximal gastric vagotomy, the effects of intravenous insulin (1 U/kg) and intravenous gastrin (1 μg/kg) on proximal gastric motility, as measured by a gastric barostat, on plasma glucose, and on plasma gastrin, as measured by radioimmunoassay, were assessed 1 hour before and for 2 hours after injection. The effects of a cholecystokinin (CCK)-A receptor antagonist and a CCK-B receptor antagonist on insulin-induced or gastrin-induced relaxation of the proximal stomach and on plasma glucose and gastrin were also determined. Intravenous insulin decreased plasma glucose (before [mean±SD], 97±5 mg/dl vs. after, 45±3 mg/dl;P<0.05), increased plasma gastrin (before, 240 ±59 pg/ml vs. peak after, 387 ±85 pg/ml;P<0.05), and relaxed the proximal stomach (100%±0% barostat volume vs. 202% ±15% volume;P<0.05). Exogenously administered gastrin also relaxed the proximal stomach without decreasing plasma glucose. CCK-B blockade diminished, but did not abolish, the gastric relaxation caused by insulin or gastrin, whereas CCK-A blockade had little effect. It was concluded that insulin-induced relaxation of the proximal stomach after proximal gastric vagotomy is mediated, in part, by vagal release of antral gastrin. Supported by National Institutes of Health Grant DK18278 and the Mayo Foundation. Presented in part at the Annual Meeting of the American Gastroenterological Association in San Diego, Calif., May 15, 1995. An abstract of this work was published inGastroenterology 108: A652, 1995.