Cholecystokinin (CCK)-induced desensitization of pancreatic enzyme secretion is mediated by low affinity CCK receptors

D Menozzi; H A Stark; J Martinez; R T Jensen; J D Gardner

doi:10.1016/0196-9781(89)90040-5

Cholecystokinin (CCK)-induced desensitization of pancreatic enzyme secretion is mediated by low affinity CCK receptors

Peptides. 1989 Mar-Apr;10(2):337-41. doi: 10.1016/0196-9781(89)90040-5.

Authors

D Menozzi¹, H A Stark, J Martinez, R T Jensen, J D Gardner

Affiliation

¹ Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892.

PMID: 2474153
DOI: 10.1016/0196-9781(89)90040-5

Abstract

CCK-8-induced desensitization of carbachol-stimulated amylase secretion occurred over a range of concentrations of CCK-8 that occupy low affinity CCK receptors. CCK-JMV-180 [BOC-Tyr(SO3)-Nle-Gly-Trp-Nle-Asp-2-phenylethylester] at concentrations up to 1 microM did not cause desensitization of enzyme secretion; however, the peptide was able to inhibit CCK-8-induced desensitization. Analysis of the relationship between receptor occupation and CCK-8-induced desensitization caused by CCK-8 and CCK-JMV-180 in combination also indicated that CCK-8-induced desensitization of carbachol-stimulated amylase secretion is caused by occupation of low affinity CCK receptors.

MeSH terms

Amylases / metabolism*
Animals
Carbachol / pharmacology
In Vitro Techniques
Kinetics
Male
Pancreas / drug effects
Pancreas / enzymology*
Rats
Rats, Inbred Strains
Receptors, Cholecystokinin / physiology*
Sincalide / metabolism
Sincalide / pharmacology*

Substances

Receptors, Cholecystokinin
Carbachol
Amylases
Sincalide