| pubmed-article:2433951 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C1825588 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C2346452 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C0028778 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C1413246 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C1416611 | lld:lifeskim |
| pubmed-article:2433951 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:2433951 | pubmed:issue | 2 Pt 2 | lld:pubmed |
| pubmed-article:2433951 | pubmed:dateCreated | 1987-3-24 | lld:pubmed |
| pubmed-article:2433951 | pubmed:abstractText | The mechanism underlying the Ba2+-induced automaticity was studied in isolated guinea pig ventricular myocytes using the whole-cell clamp method and a patch electrode. In the presence of 0.1-0.3 mM Ba2+, application of a weak depolarizing current induced repetitive firing of spontaneous action potentials. Application of tetrodotoxin or Ca2+ channel blockers and removal of external Na+ and Ca2+ did not abolish the rhythmic activity, thereby suggesting that activation of inward currents played no crucial role in the generation of this rhythmicity. Voltage-clamp studies revealed that Ba2+ blocked the inward rectifier K+ current (iK1) in a voltage- and time-dependent manner with a greater and more rapid block at more negative potentials. This Ba2+ action could quantitatively be fitted with a model of the conventional bimolecular adsorption isotherm with a voltage-dependent dissociation constant. Simulation studies using this model showed that a membrane model, in which only the iK1 system and a small leak conductance were incorporated, could reproduce an automatic activity similar to that seen experimentally. Thus, in isolated ventricular cells, the voltage- and time-dependent block of iK1 by Ba2+ appears to be one important mechanism underlying the automaticity. | lld:pubmed |
| pubmed-article:2433951 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2433951 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2433951 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:2433951 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2433951 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2433951 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2433951 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2433951 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:2433951 | pubmed:issn | 0002-9513 | lld:pubmed |
| pubmed-article:2433951 | pubmed:author | pubmed-author:MatsuuraHH | lld:pubmed |
| pubmed-article:2433951 | pubmed:author | pubmed-author:EharaTT | lld:pubmed |
| pubmed-article:2433951 | pubmed:author | pubmed-author:ImotoYY | lld:pubmed |
| pubmed-article:2433951 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2433951 | pubmed:volume | 252 | lld:pubmed |
| pubmed-article:2433951 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2433951 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2433951 | pubmed:pagination | H325-33 | lld:pubmed |
| pubmed-article:2433951 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
| pubmed-article:2433951 | pubmed:meshHeading | pubmed-meshheading:2433951-... | lld:pubmed |
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| pubmed-article:2433951 | pubmed:meshHeading | pubmed-meshheading:2433951-... | lld:pubmed |
| pubmed-article:2433951 | pubmed:year | 1987 | lld:pubmed |
| pubmed-article:2433951 | pubmed:articleTitle | Voltage- and time-dependent block of iK1 underlying Ba2+-induced ventricular automaticity. | lld:pubmed |
| pubmed-article:2433951 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2433951 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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