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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1992-2-13
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pubmed:abstractText |
The effects on the cytosolic Ca2+ concentration of activating cholecystokinin receptors on single mouse pancreatic acinar cells have been investigated using patch-clamp whole-cell recording of Ca(2+)-dependent Cl- current. We used the nonsulphated octapeptide of cholecystokinin (CCK8-NS) since the effects of even high concentrations were rapidly reversible which was not the case for the sulphated octapeptide. A submaximal concentration of CCK8-NS (10 nM) evoked a current response consisting of short-lasting (a few seconds) spikes, and some of these spikes were seen to trigger larger and longer (about half a minute) current pulses. At a higher concentration (100 nM) CCK8-NS evoked smooth and sustained responses. The effect of CCK8-NS was almost abolished when the internal perfusion solution contained a high concentration of the Ca2+ chelator EGTA (5 mM). The responses evoked by CCK8-NS were independent of the presence of Ca2+ in the external solution at least for the first 5 min of stimulation. Internal perfusion with GTP-gamma-S markedly potentiated the effect of CCK8-NS or at a higher concentration itself induced responses very similar to those normally evoked by CCK8-NS. Caffeine added to the external solution at a low concentration (0.2-1 mM) enhanced weak CCK8-NS responses, whereas high caffeine concentrations always inhibited the CCK8-NS-evoked responses. These inhibitory caffeine effects were quickly reversible. Forskolin evoked a similar inhibitory effect. Intracellular heparin (200 micrograms/ml) infusion markedly inhibited the response to CCK8-NS stimulation. We conclude that the primary effect of activating CCK receptors is to induce inositoltrisphosphate (IP3) production.(ABSTRACT TRUNCATED AT 250 WORDS)
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Caffeine,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium,
http://linkedlifedata.com/resource/pubmed/chemical/Calcium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Cholecystokinin,
http://linkedlifedata.com/resource/pubmed/chemical/Guanosine 5'-O-(3-Thiotriphosphate),
http://linkedlifedata.com/resource/pubmed/chemical/Heparin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholecystokinin,
http://linkedlifedata.com/resource/pubmed/chemical/Sulfates
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0022-2631
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
124
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
179-87
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:1662286-Animals,
pubmed-meshheading:1662286-Caffeine,
pubmed-meshheading:1662286-Calcium,
pubmed-meshheading:1662286-Calcium Channels,
pubmed-meshheading:1662286-Cholecystokinin,
pubmed-meshheading:1662286-Cytoplasm,
pubmed-meshheading:1662286-Drug Interactions,
pubmed-meshheading:1662286-Electric Conductivity,
pubmed-meshheading:1662286-Guanosine 5'-O-(3-Thiotriphosphate),
pubmed-meshheading:1662286-Heparin,
pubmed-meshheading:1662286-Mice,
pubmed-meshheading:1662286-Pancreas,
pubmed-meshheading:1662286-Perfusion,
pubmed-meshheading:1662286-Receptors, Cholecystokinin,
pubmed-meshheading:1662286-Signal Transduction,
pubmed-meshheading:1662286-Sulfates
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pubmed:year |
1991
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pubmed:articleTitle |
Cytoplasmic Ca2+ signals evoked by activation of cholecystokinin receptors: Ca(2+)-dependent current recording in internally perfused pancreatic acinar cells.
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pubmed:affiliation |
Physiological Laboratory, University of Liverpool, United Kingdom.
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pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
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