Abstract
Cardiac hypertrophy is the physiological adaptation of the heart to chronic hemodynamic overload. Hypertrophy produces an adaptational advantage both by multiplying the contractile units and by normalizing wall stress. On the other hand, hypertrophy might be detrimental. For example, the decrease of the maximum unloading velocity, beneficial at the fiber level, is detrimental in terms of diastolic function and cardiac output [reviewed in 1].
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References
Swynghedauw B (1990) Cardiac hypertrophy and failure. Paris, London INSERM J. Libbey Pub, 740 pp.
Anversa P, Loud A, Giaeomelli F et al (1978) Absolute morphometric study of myocardial hypertrophy in experimental hypertension. Lab Invest 38:597–609
Korecky B, Rakusan K (1978) Normal and hypertrophic growth of the rat heart: changes in cell dimensions and number. Am J Physiol 234: H123–H128.
Mayoux E, Callens F, Swynghedauw B, Charlemagne D (1988) Adaptational process of the cardiac Ca2+ channels to pressure overload: Biochemical and physiological properties of the DHP receptors in normal and hypertrophied rat hearts. J Cardiovasc Pharmacol 12:390–396
Primot I, Mayoux E, Oliviero P, Charlemagne D (1991) Effect of pressure overload on cardiac Ca2+ antagonist binding sites of guinea pig. Comparison with adaptational response of the hypertrophied rat heart. Cardiovasc Res 25:875–880.
Reuter H (1983) Calcium channel modulation by neurotransmitters, enzymes and drugs. Nature 301: 569–572.
Schwartz LM, Mc Clerley EW, Almers W (1985) DHP receptors in muscle and voltage– dependant but most are functionnal calcium channels. Nature 314: 747–51.
Sainte Beuve C, Leclerq C, Rannou F, Oliviero P, Mansier P, Chevalier B, Swynghedauw B, Charlemagne D (1992) Remodeling of the hypertensive heart. Kidney International 41: suppl. 37 in press.
De la Bastie D, Levitsky D, Rappaport L, Mercadier JJ, Schwartz K, Lompre AM (1990) Function of the sarcoplasmic reticulum and expression of its Ca2+ ATPase gene in pressure overload-induced cardiac hypertrophy in the rat. Circ Res 66: 554–564
Nagai R, Zarain-Herzberg A, Alpert N, Periasamy M (1989) Regulation of myocardial Ca2+ ATPase and phospholamban mRNA expression in response to pressure overload and thyroid hormone. Proc Natl Acad Sci USA 86: 2966–2970
Hanf R, Drubaix I, Lelievre LG (1988) Rat cardiac hypertrophy: altered sodium calcium exchange activity in sarcolemmal vesicles. FEBS Letters 236:145–149
Andrawis NJ, Kuoth, Giaeomelli F, Wiener J (1988) Altered calcium regulation in the cardiac plasma membrane in experimental renal hypertension. J Mol Cell Cardiol 20:625–634
Swynghedauw B (1990) Changes in membrane proteins in chronic mechanical overload of the heart. Am J Cardiol 65:30G–33G
Mansier P, Chevalier B, Mayoux E, Swynghedauw B (1990) Membrane proteins of the myocytes in cardiac overload. Br J Clin Pharmac 30: 43S–48S
Bristow MR, Anderson FL, Port DJ, Feldman A (1991) Differences in adrenergic neuroeffector mechanism in ischemic versus idiopathic dilated cardiomyopathy. Circulation 84: 1024–1039.
Orlowski, Lingrel JB (1990) Thyroid and glucocorticoid hormones regulate the expression of multiple Na, K-ATPase genes in culture neonatal rat cardiac myocytes. J Biol Chem 265:3462–3470.
Charlemagne D, Maixent JM, Preteseille J, Lelievre LG (1986) Ouabain binding sites and Na+/ K+ ATPase activity in rat cardiac hypertrophy. Expression of the neonatal form. J Biol Chem 261: 185–189.
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© 1992 Springer-Verlag Tokyo
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Leclercq, C. et al. (1992). Cellular Mechanisms of Left Ventricular Hypertrophy. In: Yasuda, H., Kawaguchi, H. (eds) New Aspects in the Treatment of Failing Heart. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68219-6_6
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DOI: https://doi.org/10.1007/978-4-431-68219-6_6
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-68221-9
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