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Increased sensitivity of gastrin release to adrenaline in duodenal ulcer.

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Serum gastrin concentrations were measured in patients with duodenal ulcer and controls before, during, and after one-hour intravenous infusion of various doses of adrenaline (0.12 microgram to 6 microgram/min). Gastrin concentrations in the basal state were significantly increased in duodenal ulcer patients compared to controls. The maximal rise in serum gastrin concentrations was obtained at a dose of 4 microgram/min adrenaline in both groups of subjects, and the increase was significantly higher in duodenal ulcer patients than in controls. Adrenaline increased predominantly the gastrin III component (gastrin-17 like) in both duodenal ulcer patients and controls. The threshold level of adrenaline-induced gastrin release was significantly lower in duodenal ulcer patients: intravenous infusion of adrenaline in a dose of 0.12 microgram and 0.25 microgram/min increased serum gastrin concentrations 23 and 43%, respectively, but had no effect in controls. Rises in plasma adrenaline concentrations were similar in both groups of subjects in response to the various doses of adrenaline employed. Only the smallest dose of adrenaline (0.12 microgram/min) resulted in clearly physiological variations in plasma adrenaline concentrations. The results indicate that endogenous adrenaline may stimulate the secretion of gastrin during physiological conditions in patients with duodenal ulcer.
Title: Increased sensitivity of gastrin release to adrenaline in duodenal ulcer.
Description:
Serum gastrin concentrations were measured in patients with duodenal ulcer and controls before, during, and after one-hour intravenous infusion of various doses of adrenaline (0.
12 microgram to 6 microgram/min).
Gastrin concentrations in the basal state were significantly increased in duodenal ulcer patients compared to controls.
The maximal rise in serum gastrin concentrations was obtained at a dose of 4 microgram/min adrenaline in both groups of subjects, and the increase was significantly higher in duodenal ulcer patients than in controls.
Adrenaline increased predominantly the gastrin III component (gastrin-17 like) in both duodenal ulcer patients and controls.
The threshold level of adrenaline-induced gastrin release was significantly lower in duodenal ulcer patients: intravenous infusion of adrenaline in a dose of 0.
12 microgram and 0.
25 microgram/min increased serum gastrin concentrations 23 and 43%, respectively, but had no effect in controls.
Rises in plasma adrenaline concentrations were similar in both groups of subjects in response to the various doses of adrenaline employed.
Only the smallest dose of adrenaline (0.
12 microgram/min) resulted in clearly physiological variations in plasma adrenaline concentrations.
The results indicate that endogenous adrenaline may stimulate the secretion of gastrin during physiological conditions in patients with duodenal ulcer.

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