© 2003 by European Society of Cardiology
Copyright © 2003, European Society of Cardiology
Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis
aDepartment of Medicine, University of Illinois at Chicago, 840 South Wood Street, M/C 787, Chicago, IL 60612, USA
bLaboratory of Experimental Cardiology, University of Leuven, Leuven, Belgium
cInterdisciplinary Research Center, University of Leuven, Kortrijk, Belgium
dDepartment of Physiology, Loyola University Chicago, Maywood, IL 60153, USA
* Corresponding author.
Received 8 July 2002; accepted 17 October 2002
KEYWORDS Arrhythmia (mechanisms); Contractile function; Heart failure; Hypertrophy; Na/H-exchanger; Na/K-pump
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1. [Na]i in hypertrophy and heart failure |
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Myocardial hypertrophy (Hyp) and heart failure (HF) are pathologic states characterized by altered intracellular Ca handling [1,2] that can contribute to diastolic and/or systolic dysfunction and arrhythmias [1,3]. However, there is an important interplay between intracellular Na ([Na]i) and Ca handling, so that altered levels of [Na]i and Na transporters can have profound effects on both contractile function and arrhythmogenesis. Both intracellular [Ca] ([Ca]i) and intracellular pH (pHi) in cardiac myocytes depend strongly on [Na]i [1]. This is because Na/Ca exchange (NCX) and Na/H exchange (NHE) are powerful transport mechanisms that use the energy stored in the transmembrane [Na] electrochemical gradient to extrude Ca and protons from the cell. Thus, when [Na]i rises it can limit the ability of NCX and NHE to extrude Ca and protons from myocytes. This could slow relaxation and recovery of pHi from acid loads (e.g. during ischemia). First let
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2. Causes of [Na]i elevation in heart failure |
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3. Functional consequences of elevated [Na]i |
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4. Changes in Ca handling in hypertrophy and heart failure |
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5. Na and arrhythmogenesis in hypertrophy and heart failure |
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6. Conclusion |
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