| pubmed-article:1662286 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1179517 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0205102 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0521449 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0034791 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1444748 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0596235 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C2003851 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0521116 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1549542 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C0851827 | lld:lifeskim |
| pubmed-article:1662286 | lifeskim:mentions | umls-concept:C1701901 | lld:lifeskim |
| pubmed-article:1662286 | pubmed:issue | 2 | lld:pubmed |
| pubmed-article:1662286 | pubmed:dateCreated | 1992-2-13 | lld:pubmed |
| pubmed-article:1662286 | 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) | lld:pubmed |
| pubmed-article:1662286 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1662286 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1662286 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1662286 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:1662286 | pubmed:issn | 0022-2631 | lld:pubmed |
| pubmed-article:1662286 | pubmed:author | pubmed-author:PetersenO HOH | lld:pubmed |
| pubmed-article:1662286 | pubmed:author | pubmed-author:KastWW | lld:pubmed |
| pubmed-article:1662286 | pubmed:author | pubmed-author:WakuiMM | lld:pubmed |
| pubmed-article:1662286 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1662286 | pubmed:volume | 124 | lld:pubmed |
| pubmed-article:1662286 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1662286 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1662286 | pubmed:pagination | 179-87 | lld:pubmed |
| pubmed-article:1662286 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:meshHeading | pubmed-meshheading:1662286-... | lld:pubmed |
| pubmed-article:1662286 | pubmed:year | 1991 | lld:pubmed |
| pubmed-article:1662286 | pubmed:articleTitle | Cytoplasmic Ca2+ signals evoked by activation of cholecystokinin receptors: Ca(2+)-dependent current recording in internally perfused pancreatic acinar cells. | lld:pubmed |
| pubmed-article:1662286 | pubmed:affiliation | Physiological Laboratory, University of Liverpool, United Kingdom. | lld:pubmed |
| pubmed-article:1662286 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1662286 | pubmed:publicationType | In Vitro | lld:pubmed |
| pubmed-article:1662286 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1662286 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1662286 | lld:pubmed |
