Mechanism of the Inhibitory Action of Endogenous Cholecystokinin and Caerulein on Pentagastrin — Induced Gastric Secretion

Abstract

In dogs with vagally innervated gastric pouches (PP), gastric fistulas, and pancreatic fistulas, half maximal response to pentagastrin has been obtained. Caerulein given intravenously in doses ranging from 60 to 500 ng/kg-hr caused a dose-related inhibition of PP response to pentagastrin with the maximum of about 72% reached at the dose of 250 ng/kg-hr caerulein. Endogenous cholecystokinin (CCK) released by intraduodenal instillation of L-leucine and L-tryptophan mixture reduced acid response from PP by about 50% and caused an increase in pancreatic protein output equal to that reached with 120 ng/kg-hr of caerulein. Following surgical conversion of PP to Heidenhain pouch (HP), endogenous CCK and doses of caerulein producing an equal rate of pancreatic protein secretion were ineffective in the inhibition of pentagastrin-induced gastric acid secretion from HP. Stimulation by pentagastrin combined with a threshold dose of Urecholine increased the susceptibility of HP to inhibition by caerulein. From these results we have tentatively concluded that the cholinergic innervation plays a direct role in the inhibition of pentagastrin-induced gastric secretion by CCK.

Key-words:

• Amino acids
• caerulein
• cholecystokinin
• gastric fistula
• Heidenhain pouch
• pancreatic fistula
• Pavlov pouch
• pentagastrin