Intracellular sodium determines frequency-dependent alterations in contractility in hypertrophied feline ventricular myocytes.
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David M. Harris | Steven R Houser | S. Houser | Xiongwen Chen | Xiongwen Chen | David M Harris | Geoffrey D Mills | Geoffrey D. Mills
[1] D. Allen,et al. Influence of stimulation frequency on [Na+]i and contractile function in Langendorff-perfused rat heart. , 1997, The American journal of physiology.
[2] Donald M. Bers,et al. Na+-Ca2+ Exchange Current and Submembrane [Ca2+] During the Cardiac Action Potential , 2002, Circulation research.
[3] C. Fry,et al. Intracellular sodium and contractile function in hypertrophied human and guinea-pig myocardium , 2001, Pflügers Archiv.
[4] Wolfgang Walz,et al. Patch-clamp applications and protocols , 1995 .
[5] Antonis A Armoundas,et al. Role of Sodium-Calcium Exchanger in Modulating the Action Potential of Ventricular Myocytes From Normal and Failing Hearts , 2003, Circulation research.
[6] K. Philipson,et al. The Na+-Ca2+ Exchanger Is Essential for the Action of Cardiac Glycosides , 2002, Circulation research.
[7] R. Coronel,et al. Increased Na+/H+-exchange activity is the cause of increased [Na+]i and underlies disturbed calcium handling in the rabbit pressure and volume overload heart failure model. , 2003, Cardiovascular research.
[8] Lars S. Maier,et al. Rate Dependence of [Na+]i and Contractility in Nonfailing and Failing Human Myocardium , 2002, Circulation.
[9] C. Balke,et al. Alterations in calcium handling in cardiac hypertrophy and heart failure. , 1998, Cardiovascular research.
[10] F. Verdonck,et al. Intracellular Na+ and altered Na+ transport mechanisms in cardiac hypertrophy and failure. , 2003, Journal of molecular and cellular cardiology.
[11] F. Verdonck,et al. Increased Na+ concentration and altered Na/K pump activity in hypertrophied canine ventricular cells. , 2003, Cardiovascular research.
[12] S. Houser,et al. Sarcoplasmic reticulum-related changes in cytosolic calcium in pressure-overload-induced feline LV hypertrophy. , 1993, The American journal of physiology.
[13] Donald M Bers,et al. Intracellular Na+ Concentration Is Elevated in Heart Failure But Na/K Pump Function Is Unchanged , 2002, Circulation.
[14] R. Vaughan-Jones,et al. The quantitative relationship between twitch tension and intracellular sodium activity in sheep cardiac Purkinje fibres. , 1984, The Journal of physiology.
[15] R. Coronel,et al. [Na+]i and the driving force of the Na+/Ca2+-exchanger in heart failure. , 2003, Cardiovascular research.
[16] B. Lorell,et al. Selective changes in cardiac gene expression during compensated hypertrophy and the transition to cardiac decompensation in rats with chronic aortic banding. , 1993, Circulation research.
[17] Donald M Bers,et al. Intracellular [Na+] and Na+ pump rate in rat and rabbit ventricular myocytes , 2002, The Journal of physiology.
[18] O. Sejersted,et al. Reduced myocardial Na+, K(+)-pump capacity in congestive heart failure following myocardial infarction in rats. , 1998, Journal of molecular and cellular cardiology.
[19] M. Diaz,et al. Variability of spontaneous Ca2+ release between different rat ventricular myocytes is correlated with Na(+)-Ca2+ exchange and [Na+]i. , 1996, Circulation research.
[20] D. Bers,et al. Intracellular Na in animal models of hypertrophy and heart failure: contractile function and arrhythmogenesis. , 2003, Cardiovascular research.
[21] David M. Harris,et al. Phosphorylation of phospholamban at threonine-17 reduces cardiac adrenergic contractile responsiveness in chronic pressure overload-induced hypertrophy. , 2006, American journal of physiology. Heart and circulatory physiology.
[22] G. Hasenfuss,et al. Alterations in intracellular calcium handling associated with the inverse force-frequency relation in human dilated cardiomyopathy. , 1995, Circulation.
[23] C. Luo,et al. A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction. , 1991, Circulation research.
[24] K. Sipido,et al. Monensin-induced reversal of positive force-frequency relationship in cardiac muscle: role of intracellular sodium in rest-dependent potentiation of contraction. , 1997, Journal of molecular and cellular cardiology.
[25] E. Erdmann,et al. Intracellular calcium handling in isolated ventricular myocytes from cardiomyopathic hamsters (strain BIO 14.6) with congestive heart failure. , 1994, Cell calcium.
[26] T. Eschenhagen,et al. Cellular and molecular aspects of contractile dysfunction in heart failure. , 1998, Cardiovascular research.
[27] E. Lakatta,et al. Intracellular calcium transients and developed tension in rat heart muscle. A mechanism for the negative interval-strength relationship , 1985, The Journal of general physiology.
[28] A. Yao,et al. Abnormal myocyte Ca2+homeostasis in rabbits with pacing-induced heart failure. , 1998, American journal of physiology. Heart and circulatory physiology.
[29] S. Houser,et al. Calcium transients in feline left ventricular myocytes with hypertrophy induced by slow progressive pressure overload. , 1992, Journal of molecular and cellular cardiology.
[30] Eric I. Rossman,et al. Abnormal frequency-dependent responses represent the pathophysiologic signature of contractile failure in human myocardium. , 2004, Journal of molecular and cellular cardiology.
[31] L. Brunton,et al. Excitation-contraction coupling and cardiac contractile force , 1992 .
[32] S. Houser,et al. Isolation and morphology of calcium-tolerant feline ventricular myocytes. , 1983, The American journal of physiology.
[33] S. Houser,et al. Voltage‐dependent Ca2+ release from the SR of feline ventricular myocytes is explained by Ca2+‐induced Ca2+ release , 2000, The Journal of physiology.
[34] R. Schwinger,et al. Sodium pump isoform expression in heart failure: implication for treatment , 2002, Basic Research in Cardiology.
[35] A. Yao,et al. Abnormal myocyte Ca 2 1 homeostasis in rabbits with pacing-induced heart failure , 1998 .
[36] N. Alpert,et al. Sarcoplasmic reticulum gene expression in pressure overload-induced cardiac hypertrophy in rabbit. , 1995, The American journal of physiology.
[37] S. Houser,et al. Abnormalities of calcium cycling in the hypertrophied and failing heart. , 2000, Journal of molecular and cellular cardiology.