期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 39, 期 1, 页码 61-70出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2005.01.005
关键词
K-ATP channel; action potential shortening; contractile failure
资金
- NHLBI NIH HHS [HL51909, HL45742] Funding Source: Medline
K-ATP channels are present at an extremely high density in the heart, and we know from in vitro studies that channel activation causes dramatic action potential shortening and contractile failure. But, if and when this happens in vivo is still a matter of debate. Twenty one years of intense study have led to a well-developed understanding of the molecular basis of K-ATP channel activity. Structure-function studies, together with cellular experiments probing regulatory molecules have told us much about the way the K-ATP channel can activate, and gene-targeting and proteomic tools have further elucidated determinants of in vivo function. However, the true physiological determinants of sarcolemmal K-ATP activity remain we still await full illumination of the role of the channel in the intact heart. (c) 2005 Elsevier Ltd. All rights reserved.
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