To examine the role of
gastrin as a major mediator of meal-stimulated
acid secretion at low and high intragastric pH, gastric acid secretory responses after exogenous and endogenous stimulation were studied in relation to circulating plasma
gastrin levels in 19 healthy control subjects and in 18 patients with inactive
duodenal ulcer disease.
Gastrin was given intravenously in stepwise fourfold-increasing doses from 3.1 to 800 pmol.kg-1.h-1 over consecutive 30-minute periods. Circulating plasma
gastrin and
acid secretion rates, measured by intragastric titration, were compared with the values obtained during endogenous stimulation by intragastric meals of 0.5, 1, 2, 4, and 8 g%
peptone at either pH 5.5 or pH 2.5. The studies showed that circulating
gastrin is a major regulator of
acid secretion in the presence of
peptone in both healthy controls and subjects with
duodenal ulcers. Patients with
duodenal ulcers had higher
acid secretion rates in response to endogenous and exogenous stimulation. In
duodenal ulcer subjects and healthy controls,
acid secretion in response to higher doses (2-8 g%) of
peptone was inhibited at low intragastric pH. This pH inhibition could be fully explained by diminished
gastrin release. Patients in the DU group differed from the controls by diminished inhibition of
acid secretion at intragastric pH 2.5 when low doses (1 g%) of
peptone meals were used. In summary,
gastrin is a major regulator of endogenously stimulated
acid secretion at high and low intragastric pH in healthy subjects. DU patients differ from healthy controls by higher total
acid secretion rates and diminished inhibition of
acid secretion when low concentrations of
peptone are present in the stomach.