Experimental pancreatitis is mediated by low-affinity cholecystokinin receptors that inhibit digestive enzyme secretion

A. K. Saluja, M. Saluja, H. Printz, A. Zavertnik, A. Sengupta, M. L. Steer

Research output: Contribution to journalArticle

93 Scopus citations

Abstract

Rats infused with a supramaximally stimulating dose of the cholecystokinin (CCK) analog caerulein develop acute edematous pancreatitis. Using CCK-JMV-180, a recently developed CCK analog that acts as an agonist at high-affinity CCK receptors but antagonizes the effect of CCK at low-affinity receptors, we have determined that caerulein induces pancreatitis by interacting with low-affinity CCK receptors. Those low-affinity receptors mediate CCK-induced inhibition of digestive enzyme secretion from the pancreas. Our observations, therefore, suggest that this form of experimental pancreatitis results from the inhibition of pancreatic digestive enzyme secretion.

Original languageEnglish (US)
Pages (from-to)8968-8971
Number of pages4
JournalProceedings of the National Academy of Sciences of the United States of America
Volume86
Issue number22
DOIs
StatePublished - 1989

Keywords

  • cathepsin B
  • exocrine secretion
  • lysosomes

ASJC Scopus subject areas

  • General

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