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
Gastroenterologyjournal_title
Gastroenterologyauthors
Watanabe S,Takeuchi T,Chey WYdoi
10.1016/0016-5085(92)90111-bsubject
Has Abstractpub_date
1992-02-01 00:00:00pages
621-8issue
2eissn
0016-5085issn
1528-0012pii
0016-5085(92)90111-Bjournal_volume
102pub_type
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