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

Abstract:

: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 camostat-induced increase in pancreatic secretion; volume and bicarbonate output were reduced by 35% each and amylase output by 73%. The combined administration 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.

journal_name

Gastroenterology

journal_title

Gastroenterology

authors

Watanabe S,Takeuchi T,Chey WY

doi

10.1016/0016-5085(92)90111-b

subject

Has Abstract

pub_date

1992-02-01 00:00:00

pages

621-8

issue

2

eissn

0016-5085

issn

1528-0012

pii

0016-5085(92)90111-B

journal_volume

102

pub_type

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