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Na+ i handling in the failing human heart Pieske B; Houser SRCardiovasc Res 2003[Mar]; 57 (4): 874-86Proper 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.|Animals[MESH]|Calcium/metabolism[MESH]|Heart Failure/*metabolism[MESH]|Humans[MESH]|Mammals/metabolism[MESH]|Myocardial Contraction/physiology[MESH]|Myocytes, Cardiac/metabolism[MESH]|Sodium/*metabolism[MESH] |
