The effect of
bombesin, a possible
neurotransmitter of
gastrin release, upon
gastrin and gastric acid secretion was investigated in 25 patients with
duodenal ulcer and in 16 normal subjects. In patients with
duodenal ulcer bombesin (10 ng/kg/min) produced an increase in plasma
gastrin output (median 22.4 (range 7.5-75.8) pmol/l/min) similar to that obtained in normal subjects (median 24.4 (range 5.8-56.5) pmol/l/min), whereas
gastrin stimulated by a meal was significantly higher in the group of patients with
duodenal ulcer (median 20.7 (range 9.2-42.9) vs 16.2 (range 3.4-22.2) p<0.05). Peak
acid output induced by
bombesin was significantly higher in patients with
duodenal ulcer than in normal subjects (median 24.4 (range 9.0-63.8) vs 14.0 (range 3.0-24.8) mmol/h, p<0.05) despite identical
gastrin outputs. The ratio (%) obtained by dividing the
acid secretory response to
bombesin by the response to
pentagastrin, however, was similar in both normal subjects and patients with
duodenal ulcer (median 55 (range 20-116) vs 58 (range 31-95) respectively). The difference between the
gastrin response to food and
bombesin could be explained by the fact that
bombesin releases
gastrin directly, whereas a
protein meal involves several mechanisms (neural, peptidergic, paracrine, endocrine), either stimulatory or inhibitory. The above results indicate that a higher concentration in
antral and/or duodenal
gastrin is unlikely to be present in patients with
duodenal ulcer. An increased parietal cell mass could explain the higher gastric acid response after
bombesin infusion in our group of patients with
duodenal ulcer.