| pubmed-article:9336346 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0006675 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0034721 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0034693 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C1522565 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C1515877 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0679622 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0205314 | lld:lifeskim |
| pubmed-article:9336346 | lifeskim:mentions | umls-concept:C0246904 | lld:lifeskim |
| pubmed-article:9336346 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:9336346 | pubmed:dateCreated | 1997-11-3 | lld:pubmed |
| pubmed-article:9336346 | pubmed:abstractText | Levosimendan, a new Ca++-sensitizing and positive inotropic agent, was reported to act as a coronary vasodilator and protect ischemic myocardium. To elucidate the mechanisms of these actions, the possible electrophysiological effects of levosimendan on isolated rat ventricular cells were examined by the patch-clamp technique with whole-cell and single-channel recordings. Levosimendan (3 and 10 microM) markedly shortened action potential duration and activated an outward current at potentials positive to -70 mV. The increased current was abolished by glibenclamide, a blocker of the ATP-sensitive K+ (K[ATP]) current. Stimulation of K[ATP] current was dose dependent, with an EC50 value of 4.7 microM; a maximal effect occurred at 30 microM. The L-type Ca++ current was not affected by levosimendan (0.2-10 microM). In single-channel current recording in open cell-attached patches, K[ATP] channels, which had been inhibited by 0.3 mM ATP, were activated by levosimendan. However, levosimendan did not stimulate the K[ATP] channels that exhibited high spontaneous activity in ATP-free solution. Levosimendan also could not stimulate K[ATP] channels that had rundown in ATP-free solution. However, levosimendan could stimulate rundown K[ATP] channels that were reactivated by nucleotide diphosphates. K[ATP] channels inhibited by 0.5 mM AMP-PNP, a nonhydrolyzable ATP analog, were not stimulated by levosimendan; however, the channels were stimulated by levosimendan in the presence of 30 to 50 microM ADP. Levosimendan stimulates cardiac K[ATP] channels that are suppressed by intracellular ATP. It appears that levosimendan acts synergistically with nucleotide diphosphates. These properties of levosimendan may help protect ischemic myocardium because activation of K[ATP] channels by levosimendan would likely occur in ischemic regions in which intracellular ADP concentration is increased and intracellular ATP concentration is decreased. | lld:pubmed |
| pubmed-article:9336346 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9336346 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9336346 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9336346 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9336346 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9336346 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:9336346 | pubmed:issn | 0022-3565 | lld:pubmed |
| pubmed-article:9336346 | pubmed:author | pubmed-author:SperelakisNN | lld:pubmed |
| pubmed-article:9336346 | pubmed:author | pubmed-author:KatsubeYY | lld:pubmed |
| pubmed-article:9336346 | pubmed:author | pubmed-author:SunagawaMM | lld:pubmed |
| pubmed-article:9336346 | pubmed:author | pubmed-author:YokoshikiHH | lld:pubmed |
| pubmed-article:9336346 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9336346 | pubmed:volume | 283 | lld:pubmed |
| pubmed-article:9336346 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9336346 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9336346 | pubmed:pagination | 375-83 | lld:pubmed |
| pubmed-article:9336346 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:9336346 | pubmed:meshHeading | pubmed-meshheading:9336346-... | lld:pubmed |
| pubmed-article:9336346 | pubmed:year | 1997 | lld:pubmed |
| pubmed-article:9336346 | pubmed:articleTitle | The novel calcium sensitizer levosimendan activates the ATP-sensitive K+ channel in rat ventricular cells. | lld:pubmed |
| pubmed-article:9336346 | pubmed:affiliation | Department of Molecular and Cellular Physiology, College of Medicine, University of Cincinnati, Ohio 45267-0576, USA. yokoshh@ucbeh.san.uc.edu | lld:pubmed |
| pubmed-article:9336346 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:9336346 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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