Selected Publication:
Pieske, B; Houser, SR.
Na+i handling in the failing human heart.
Cardiovasc Res. 2003; 57(4):874-886
Doi: 10.1016/S0008-6363(02)00841-6
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- Leading authors Med Uni Graz
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Pieske Burkert Mathias
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- Abstract:
- Proper contractile function of the heart depends on intact excitation-contraction processes and ion homeostasis of the myocytes. The Ca2+ ion activates contraction through its binding to troponin C. However, Ca2+ homeostasis is tightly linked to Na+ regulation because the primary mechanism for Ca2+ efflux in cardiac myocytes is via electrogenic Na+/Ca2+-exchange. While altered Ca2+-homeostasis has been demonstrated in animal models of heart failure and failing human cardiac tissue, the role of dysfunctional Na+ handling processes in altered excitation-contraction coupling remains obscure. Furthermore, altered Na+ handling has been implicated in a wide range of cellular processes, such as regulation of membrane potential, pH, and growth. This review will discuss (1) the evidence for altered [Na+]i homeostasis in the failing human heart, (2) how alterations in the Na+ electrochemical gradient can influence Ca2+ handling, contractile function, and a number of other cellular processes, and (3) the potential defects in Na+ channels and transporters that may underlie altered [Na+]i in the failing human heart.
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Animals -
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Calcium - metabolism
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Heart Failure, Congestive - metabolism
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Humans - metabolism
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Mammals - metabolism
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Myocardial Contraction - physiology
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Myocytes, Cardiac - metabolism
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Sodium - metabolism
- Find related publications in this database (Keywords)
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calcium (cellular)
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contractile function
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heart failure
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myocytes
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Na/Ca-exchanger