Source:http://linkedlifedata.com/resource/pubmed/id/11101197
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2001-2-23
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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.
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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/5-hydroxydecanoic acid,
http://linkedlifedata.com/resource/pubmed/chemical/Anti-Arrhythmia Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Benzamides,
http://linkedlifedata.com/resource/pubmed/chemical/Bradykinin,
http://linkedlifedata.com/resource/pubmed/chemical/Decanoic Acids,
http://linkedlifedata.com/resource/pubmed/chemical/HMR 1098,
http://linkedlifedata.com/resource/pubmed/chemical/Hydroxy Acids,
http://linkedlifedata.com/resource/pubmed/chemical/Potassium Channels,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Bradykinin B2,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Bradykinin
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0920-3206
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
14
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
497-502
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11101197-Analysis of Variance,
pubmed-meshheading:11101197-Animals,
pubmed-meshheading:11101197-Anti-Arrhythmia Agents,
pubmed-meshheading:11101197-Benzamides,
pubmed-meshheading:11101197-Bradykinin,
pubmed-meshheading:11101197-Decanoic Acids,
pubmed-meshheading:11101197-Hemodynamics,
pubmed-meshheading:11101197-Hydroxy Acids,
pubmed-meshheading:11101197-Male,
pubmed-meshheading:11101197-Myocardial Infarction,
pubmed-meshheading:11101197-Organ Size,
pubmed-meshheading:11101197-Potassium Channels,
pubmed-meshheading:11101197-Rabbits,
pubmed-meshheading:11101197-Receptor, Bradykinin B2,
pubmed-meshheading:11101197-Receptors, Bradykinin
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pubmed:year |
2000
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pubmed:articleTitle |
Infarct size limitation by bradykinin receptor activation is mediated by the mitochondrial but not by the sarcolemmal K(ATP) channel.
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pubmed:affiliation |
Second Department of Internal Medicine, Sapporo Medical University School of Medicine, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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