Duodenal acidification is known to inhibit gastric H+ secretion while stimulating pancreatic HCO-3 secretion, but the mechanisms of these effects have not been fully explained. This study was designed to determine the role of endogenous and exogenous
secretin in gastric inhibition and pancreatic stimulation by an acidified liver extract (LE) meal in conscious dogs prepared with chronic gastric and
pancreatic fistulas pretreated with normal serum (control) or anti-
secretin serum. In control tests, plasma
gastrin and gastric H+ secretion showed a marked rise with LE meals at pH ranging from 7.0 to 4.0, but significantly declined at pH 3.0 and 2.0. Plasma
secretin and pancreatic secretion started to rise with LE meals at pHs below 4.5, and both reached peaks at pH 2.0. Exogenous
secretin infused at graded doses suppressed plasma
gastrin and gastric H+ responses to LE meals at doses of 1.0 and 2.0 U/kg-h, but increased, dose-dependently, plasma
secretin and pancreatic HCO-3 starting with a dose of 0.03 U/kg-h. Following the administration of anti-
secretin serum, the effects of exogenous
secretin on plasma
gastrin and
secretin levels as well as on gastric and pancreatic secretion were almost completely abolished. The increase in plasma
secretin and pancreatic HCO-3 responses to LE meals at pH below 4.5 were also abolished by anti-
secretin serum, but the suppression of plasma
gastrin level and the inhibition of gastric H+ responses to LE meals at lower pH (3.0 and 2.0) remained virtually unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)