Abstract
Injection of various trypsin inhibitors into the lumen of the isolated perfused rat duodenum increased the amount of biologically active cholecystokinin-pancreozymin (CCK-BA) in the vascular perfusate. The potency to induce CCK-BA release of the various trypsin inhibitors differed. Injection of ethyl p-(6-guanidinohexanoyloxy) benzoate methanesulfonate (FOY-007; 100μmol), p-ethoxy-carbamoyl-thio-6-guanidino caproate phosphate (FOY-129; 110μmol), 4-(4-guanidinobenzoyloxy) phenylacetic acid (FOY-251; 128μmol), N, N-dimethylcarbamoylmethyl-4-(4-guanidinobenzoyloxy) phenylacetate methanesulfonate (FOY-305; 80μmol), and p-aminobenzamidine dihydrochloride (p-ABA, Sigma; 300μmol) caused release of CCK-BA amounting to 1, 042, 247, 252, 682, and 302pM, respectively. The potency to induce CCK-BA release was not correlated with the potency to inhibit trypsin activity. The present results do not support the hypothesis that a negative feed-back regulation of pancreatic enzyme secretion is exerted by intraluminal trypsin in the rat.
