期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 61, 期 -, 页码 28-33出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2013.06.001
关键词
Sodium calcium exchanger; Calcium; Heart contractility; Excitation contraction coupling; Heart failure; Genetically modified mice
资金
- Doroty and E. Phillip Lyan Endowment in Laser Research
- AHA [12IRG9140020]
- NIH [R01HL70828, R01HL48509]
Sodium-calcium exchange (NCX) is the major calcium (Ca) efflux mechanism of ventricular cardiomyocytes. Consequently the exchanger plays a critical role in the regulation of cellular Ca content and hence contractility. Reductions in Ca efflux by the exchanger, such as those produced by elevated intracellular sodium (Na) in response to cardiac glycosides, raise sarcoplasmic reticulum (SR) Ca stores. The result is an increased Ca transient and cardiac contractility. Enhanced Ca efflux activity by the exchanger, for example during heart failure, may reduce diadic cleft Ca and excitation-contraction (EC) coupling gain. This aggravates the impaired contractility associated with SR Ca ATPase dysfunction and reduced SR Ca load in failing heart muscle. Recent data from our laboratories indicate that NCX can also impact the efficiency of EC coupling and contractility independent of SR Ca load through diadic cleft priming with Ca during the upstroke of the action potential. This article is part of a Special Issue entitled Na+ Regulation in Cardiac Myocytes. (C) 2013 Elsevier Ltd. All rights reserved.
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