Stimulation of Gastrin Release and Gastric Secretion: Effect of Bombesin and a Nonapeptide in Fistula Dogs with and without Fundic Vagotomy

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Abstract
Bombesin and a synthetic bombesin nonapeptide were studied by intravenous infusion at a dose of 0.5 μg·kg-1 •h-1 for 4 h in 7 dogs with esophagostomy and gastric fistula. In 3 of the dogs who had highly selective (fundic) vagotomy, mean integrated gastrin output over 4 h was double that in the 4 dogs with vagi intact during both nonapeptide (1,554 vs. 700 pg·ml-1 •4 h-1) and bombesin infusion (2,442 vs. 1,440 pg • ml-1 • 4 h-1). Peak concentrations of serum gastrin reached during bombesin (490 ± 100 vs. 320 ± 90) were higher than those during nonapeptide infusion (270 ± 40 vs. 160 ± 28 pg/ml) in the vagotomized and intact dogs, respectively. The difference between vagotomized and vagally intact dogs suggests that the fundic vagotomy removed an inhibitor of gastrin release from the innervated antrum. Despite these differences in gastrin release, gastric acid output with the two peptides was the same (49–52 mEq/4 h) whether the fundus was denervated or innervated. This suggests that bombesin may stimulate gastric acid secretion by the release of an additional secretagogue which is not measured by the gastrin assay. Neither of the two inhibitors of gastrin release – antral acidification to pH 1.4 or less or atropine (100 μg/kg) – inhibited gastrin release by bombesin, even though the atropine reduced acid output by 80%. Bombesin is a potent gastric stimulus whose action is only partly explained by the measured gastrin release.