pubmed-article:11101197 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0021308 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0521451 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0001480 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0107053 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0456389 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C1514758 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0449295 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0439799 | lld:lifeskim |
pubmed-article:11101197 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
pubmed-article:11101197 | pubmed:issue | 5 | lld:pubmed |
pubmed-article:11101197 | pubmed:dateCreated | 2001-2-23 | lld:pubmed |
pubmed-article:11101197 | pubmed:abstractText | Earlier studies have shown that activation of bradykinin B2 receptor triggers protein kinase C (PKC)-mediated cardioprotective mechanism in ischemic preconditioning (PC). In the present study, we examined whether the effector in this B2-receptor triggered pathway of PC is the ATP sensitive potassium (K(ATP)) channel in the mitochondria (mito-K(ATP) channel) or K(ATP) channel in the sarcolemma (sarc-K(ATP) channel). Isolated rabbit hearts were perfused with modified Krebs-Henseleit buffer in a Langendorff mode, and regional myocardial ischemia was induced by occluding a left coronary artery for 30 min and then reperfusing for 2 hours. Infarct size was determined by triphenyltetrazolium chloride staining and expressed as a percentage of area at risk (% IS/AR). Infusion of bradykinin (500 nmol/L) for 15 min prior to ischemia significantly reduced % IS/AR from 37.4 +/- 2.9 (SE) of the untreated controls to 12.0 +/- 3.3%. This protective effect of bradykinin was completely abolished by coinfusion of 5-hydroxydecanoate (5-HD, 50 micromol/L), a selective mito-K(ATP) channel blocker (% IS/AR = 44.2 +/- 6.4). In contrast, a high dose of HMR1098 (20 micromol/L), which is a newly developed sarc-K(ATP) channel selective blocker with IC50 of 0.6 micromol/L, failed to modify the infarct size limitation by preischemic infusion of bradykinin (% IS/AR = 11.7 +/- 3.4). Neither 5-HD nor HMR1098 alone modified infarct size (% IS/AR = 37.8 +/- 3.8 and 35.1 +/- 6.2, respectively). These results suggest that opening of the mito-K(ATP) channel but not the sarc-K(ATP) channel is involved in infarct size limitation by a mechanism triggered by bradykinin B2 receptor activation. | lld:pubmed |
pubmed-article:11101197 | pubmed:language | eng | lld:pubmed |
pubmed-article:11101197 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11101197 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11101197 | pubmed:month | Oct | lld:pubmed |
pubmed-article:11101197 | pubmed:issn | 0920-3206 | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:KitaHH | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:MiuraTT | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:MikiTT | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:ShimamotoKK | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:TannoMM | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:FukumaTT | lld:pubmed |
pubmed-article:11101197 | pubmed:author | pubmed-author:GendaSS | lld:pubmed |
pubmed-article:11101197 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11101197 | pubmed:volume | 14 | lld:pubmed |
pubmed-article:11101197 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11101197 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11101197 | pubmed:pagination | 497-502 | lld:pubmed |
pubmed-article:11101197 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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pubmed-article:11101197 | pubmed:year | 2000 | lld:pubmed |
pubmed-article:11101197 | pubmed:articleTitle | Infarct size limitation by bradykinin receptor activation is mediated by the mitochondrial but not by the sarcolemmal K(ATP) channel. | lld:pubmed |
pubmed-article:11101197 | pubmed:affiliation | Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Japan. | lld:pubmed |
pubmed-article:11101197 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11101197 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:11101197 | lld:pubmed |