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Protection conferred by myocardial ATP-sensitive K(+) channels in pressure overload-induced congestive heart failure revealed in KCNJ11 Kir6.2-null mutant
Ventricular load can precipitate development of the heart failure syndrome, yet the molecular components that control the cardiac adaptive response to imposed demand remain partly understood. Compromised ATP-sensitive K(+) (K(ATP)) channel function renders the heart vulnerable to stress, implicating...
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| 主要な著者: | , , , , , , , , |
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| フォーマット: | Artigo |
| 言語: | Inglês |
| 出版事項: |
Blackwell Science Inc
2006
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| 主題: | |
| オンライン･アクセス: | https://ncbi.nlm.nih.gov/pmc/articles/PMC1890387/ https://ncbi.nlm.nih.gov/pubmed/17038430 https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1113/jphysiol.2006.119511 |
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