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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-6-5
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pubmed:abstractText |
Cholecystokinin octapeptide (CCK-8) is a potent corticotroph secretagogue. Consistent with earlier reports, the present results demonstrate that CCK-8 administration to rats elevates circulating beta-endorphin and adrenocorticotropin, but not alpha-melanocyte-stimulating hormone concentrations. This response was blocked by dexamethasone pretreatment, but not by vagotomy, and it could not be reproduced by i.c.v. CCK-8 injection, evidence that CCK-8 exerts its effects by directly activating cholecystokinin (CCK) receptors localized on anterior pituitary corticotrophs rather than in brain or the vagus nerve. Subsequent experiments demonstrated further that type A CCK receptors primarily mediate the stimulatory effect of CCK-8 on corticotroph secretion. Thus, devazepide, a selective CCK-A receptor antagonist, produced a dose-related inhibition of the CCK-8-stimulated rise in circulating beta-endorphin concentrations. Less selective CCK-A antagonists, including proglumide and lorglumide, produced little or no effect, however. Unexpectedly, the CCK-B receptor antagonist, L-365,260, enhanced the response to CCK-8, an effect diametrically opposite to that produced by CCK-A antagonists. These observations indicate that CCK-A and CCK-B receptors mediate quite different, if not opposing, roles in regulating corticotroph secretion.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Benzodiazepinones,
http://linkedlifedata.com/resource/pubmed/chemical/Cholecystokinin,
http://linkedlifedata.com/resource/pubmed/chemical/Devazepide,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholecystokinin,
http://linkedlifedata.com/resource/pubmed/chemical/Sincalide,
http://linkedlifedata.com/resource/pubmed/chemical/Tetragastrin,
http://linkedlifedata.com/resource/pubmed/chemical/beta-Endorphin
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0022-3565
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
261
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
454-61
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1578360-Animals,
pubmed-meshheading:1578360-Benzodiazepinones,
pubmed-meshheading:1578360-Cholecystokinin,
pubmed-meshheading:1578360-Devazepide,
pubmed-meshheading:1578360-Dose-Response Relationship, Drug,
pubmed-meshheading:1578360-Injections, Intraperitoneal,
pubmed-meshheading:1578360-Injections, Intraventricular,
pubmed-meshheading:1578360-Male,
pubmed-meshheading:1578360-Pituitary Gland,
pubmed-meshheading:1578360-Radioimmunoassay,
pubmed-meshheading:1578360-Rats,
pubmed-meshheading:1578360-Rats, Inbred Strains,
pubmed-meshheading:1578360-Receptors, Cholecystokinin,
pubmed-meshheading:1578360-Sincalide,
pubmed-meshheading:1578360-Tetragastrin,
pubmed-meshheading:1578360-Vagotomy,
pubmed-meshheading:1578360-beta-Endorphin
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pubmed:year |
1992
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pubmed:articleTitle |
Cholecystokinin type A and type B receptor antagonists produce opposing effects on cholecystokinin-stimulated beta-endorphin secretion from the rat pituitary.
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pubmed:affiliation |
Division of Molecular Biology and Biochemistry, University of Missouri-Kansas City.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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