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Mediation of trypsin inhibitor-induced pancreatic hypersecretion by secretin and cholecystokinin in rats

1992; Elsevier BV; Volume: 102; Issue: 2 Linguagem: Inglês

10.1016/0016-5085(92)90111-b

1528-0012

Shinichiro Watanabe, Tadashi Takeuchi, William Y. Chey,

Regulation of Appetite and Obesity

We investigated a hormonal mechanism in a trypsin inhibitor-induced pancreatic hypersecretion in rats.Intraduodenal administration of a synthetic trypsin inhibitor, camostat, resulted in significant increases in plasma concentration of both secretin and cholecystokinin in a dose-related manner that paralleled a significant increase in exocrine pancreatic secretion.To eliminate the effect of circulating secretin in rats, a rabbit antisecretin serum was given IV that resulted in a 77% reduction in bicarbonate secretion stimulated by intraduodenal camostat.A cholecystokinin receptor antagonist, MK-329, also inhibited significantly the camostatinduced increase in pancreatic secretion; volume and bicarbonate output were reduced by 35% each and amylase output by 73%.The comhinedadministration of antisecretin serum and MK-329 completely abolished the pancreatic exocrine secretion stimulated by camostat.These observations indicate that the camostat-stimulated pancreatic exocrine secretion is mediated by the increased release of both secretin and cholecystokinin in rats. Materials and Methods ChemicalsCamostat (FOY-305) [N,N-dimethylcarbamoylmethyl-4(4-guanidinobenzoyloxy) phenylacetate methanesul-