The role of secretin in the inhibition of gastric secretion by intraduodenal acid

The effect of intraduodenal acid on pentagastrin-stimulated gastric secretion has been investigated in 12 normal subjects and 23 patients with chronic duodenal ulceration. Plasma secretin levels were monitored during each test using a highly sensitive radioimmunoassay.Significant inhibition of gastric secretion occurred in the normal subjects and duodenal ulcer patients. A significant rise in plasma secretin was observed in both groups after intraduodenal acid though there was a complete lack of correlation between the magnitude of the secretin response and the degree of gastric inhibition. Ten subjects received intraduodenal acid and a subsequent intravenous infusion of exogenous secretin (0.125-0.25 units/kg over six minutes). Gastric inhibition occurred after the acid instillation but not after secretin infusion despite plasma secretin levels greatly in excess of those produced by intraduodenal acid.These results suggest that release of secretin by itself cannot explain the gastric inhibitory response to intraduodenal acid in man.     

The pancreas and gastric secretion: failure of pancreatectomy to prevent inhibition of gastric secretion by secretin

A second commercially prepared secretin has been found to inhibit the acid secreted by Heidenhain pouches in dogs in response to a meal but not to histamine. This inhibition is not affected by pancreatectomy.     

Inhibition of human gastric acid secretion by peptide YY and secretin

In 6 healthy volunteers we investigated the effect of secretin and peptide YY (PYY) on gastric acid secretion stimulated by pentagastrin (100 ng/kg/h). Secretin (0.05 CU/kg/h) and PYY (10.0 pmol/kg/h) were given intravenously either alone or in combination. Given alone secretin and PYY inhibited gastric acid output by 25 and 21%, respectively. The combined infusion of secretin and PYY inhibited acid output by 38% indicating an additive effect. The infusion of one hormone did not influence release of the other. It is suggested that the interaction of PYY and secretin on pentagastrin-stimulated gastric acid secretion in normal man is of the additive type.     

Effect of low-dose exogenous secretin and somatostatin on pentagastrin-stimulated gastric acid secretion in man

The inhibitory effect of intravenous infusion of secretin (0.05 CU kg-1h-1) and somatostatin (60 pmol kg-1h-1), given alone or in combination, on pentagastrin-stimulated (100 ng kg-1 h-1) acid secretion was studied in 10 healthy subjects. Secretin inhibited acid secretion by 54% (p less than 0.05), and somatostatin inhibited by 70% (p less than 0.05). The combined infusion of secretin and somatostatin decreased acid output by 64% (p less than 0.05). The differences between the three groups were not significant (p greater than 0.05). Median plasma concentrations of secretin and somatostatin were of the same magnitude as seen after duodenal acidification. The present study did not demonstrate any interaction between secretin and somatostatin in the inhibition of gastric acid secretion.     

Effect of low-dose exogenous secretin on pentagastrin- and meal-stimulated gastric acid secretion in humans

Intravenous infusion of secretin in a dose of 0.05 CU/kg/hr inhibited pentagastrin-stimulated (100 ng/kg/hr) acid secretion by 42% (P<0.05) abd meal-stimulated (10% peptone, pH 5.5) acid secretion by 33% (P<0.05) in 10 healthy subjects. Median serum gastrin concentration during peptone stimulation was reduced by 24% (P<0.05) during secretin infusion. Median plasma secretin concentrations were 6.0 and 5.2 pmol/liter, respectively. Since these secretin concentrations are of the same magnitude as those seen after duodenal acidification, it is concluded that secretin may participate in the physiological inhibition of gastric acid secretion.Supported by grant 12-4525, Danish Medical Research Council     

Effects of secretin on gastric secretion

Summary The effect of secretin on gastric secretory activity was studied in three dogs with Heidenhain pouches. A secretory plateau was elicited either by meat-feeding or by continuous administration of histamine. The effects of secretin were evaluated by comparison with identically performed control experiments in which saline alone was administered. Secretin inhibited free acid output by an average of 66% (single dose) and 51% (continuous injection), but even in large doses did not alter histamine-stimulated secretion. Inhibition by secretin was not affected by pancreatic-duct ligation. It is concluded that secretin (1) is a potent gastric secretory inhibitor; (2) is not the agent mediating gastric inhibition by fat or acid; (3) does not affect gastric secretion via the exocrine pancreas.Supported, in part, by N.I.H. Grants A-5713 and AM-5730-02 and American Cancer Society Grant E-186 B.