Abstract
Myocardial hypertrophy is associated with a number of heart diseases and is of great clinical relevance. Despite many research efforts, the signals involved in the hypertrophy process are still poorly understood (1–4). Recently, it was found that the subcellular structure of the myocyte differs in various forms of hypertrophy. Great emphasis has been placed on gene expression of the myosin heavy chains (MHC) which determine the isoenzyme population of myosin. The myosin isoenzymes influence the ATPase activity (5,6), the energetics of the cross bridge cycle (7,8), oxygen consumption of the whole heart (9,10) and the mechanics of heart muscle (11–13). Although changes in the MHC expression are less relevant for the heart of large mammals with predominantly V3, they nonetheless provide the unique possibility of tracing an altered mechanical performance of the heart to an altered gene expression. Because there is increasing evidence that in a number of functional states the MHC expression is associated with coordinated changes in the activity of the Ca2+-stimulated ATPase of sarcoplasmic reticulum (14,15), a better understanding of the regulation of gene expression of myosin should help also in understanding the regulation of the activity of the sarcoplasmic reticulum Ca2+-pump.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Zak R (ed): Growth of the Heart in Health and Disease. New York, Raven Press, 1983
Zak R: The role of protein synthesis and degradation in determining the protein composition of myocardial cells, in Rupp H (ed): The Regulation of Heart Function. New York, Stuttgart, Thieme Inc, 1986, pp 249–260
Morgan HE, Chua BHL, Watson PA, Russo L: Protein synthesis and degradation, in Fozzard HA, Haber E, Jennings RB, Katz AM, Morgan HE (eds): The Heart and Cardiovascular System. New York, Raven Press, 1986, pp 931–948
Cooper G: Cardiocyte adaptation to chronically altered load. Annu Rev Physiol 1987; 49: 501–518
Pope B, Hoh JFY, Weeds A: The ATPase activities of rat cardiac myosin isoenzymes. FEBS Lett 1980; 118: 205–208
Rupp H: Polymorphic myosin as the common determinant of myofibrillar ATPase in different haemodynamic and thyroid states. Basic Res Cardiol 1982; 77: 34–46
Holubarsch Ch, Goulette RP, Litten RZ, Martin BJ, Mulieri LA, Alpert NR: The economy of isometric force development, myosin isoenzyme pattern and myofibrillar ATPase activity in normal and hypothyroid rat myocardium. Circ Res 1985; 56: 78–86
Alpert NR, Mulieri LA: Intrinsic determinants of myocardial energetics in normal and hypertrophied hearts, in Rupp H (ed): The Regulation of Heart Function. New York, Stuttgart, Thieme Inc, 1986, pp 292–304
Kissling G, Rupp H, Malloy L, Jacob R: Alterations in cardiac oxygen consumption under chronic pressure overload. Significance of the isoenzyme pattern of myosin. Basic Res Cardiol 1982; 77: 255–269
Kissling G, Rupp H: The influence of myosin isoenzyme pattern on increase in myocardial oxygen consumption induced by catecholamines. Basic Res Cardiol 1986; 81 (suppl 1): 103–115
Schwartz K, Lecarpentier Y, Martin JL, Lompre AM, Mercadier JJ, Swynghedauw B: Myosin isoenzymic distribution correlates with speed of myocardial contraction. J Mol Cell Cardiol 1981; 13: 1071–1075
Ebrecht G, Rupp H, Jacob R: Alterations of mechanical parameters in chemically skinned preparations of rat myocardium as a function of isoenzyme pattern of myosin. Basic Res Cardiol 1982; 77: 220–234
Jacob R: Cardiac responses to experimental chronic pressure overload, in Zanchetti A, Tarazi RC (eds): Handbook of Hypertension, Vol 7: Pathophysiology of Hypertension–Cardiovascular Aspects. Amsterdam, Elsevier Science Publishers, 1986, pp 59–83
Rupp H, Wahl R, Jacob R: Remodelling of the myocyte at a molecular level–relationship between myosin isoenzyme population and sarcoplasmic reticulum, in Dhalla NS, Pierce GN, Beamish RE (eds): Heart Function and Metabolism. Boston, Martinus Nijhoff Publishing, 1987, pp 307–318
Rupp H, Jacob R, Dhalla NS: Coordinated regulation of the subcellular structures of the heart and the consequences for assessing cardiac contractility, in Jacob R (ed): Evaluation of Cardiac Contractility. Stuttgart/New York, Gustav Fischer Verlag, 1989, in press
Everett AW, Sinha AM, Umeda PK, Jakovcic S, Rabinowitz M, Zak R: Regulation of myosin synthesis by thyroid hormone: Relative change in the alpha-and beta-myosin heavy chain mRNA levels in rabbit heart. Biochemistry 1984; 23: 1596–1599
Mandavi V, Izumo S, Nadal-Ginard B: Developmental and hormonal regulation of sarcomeric myosin heavy chain gene family. Circ Res 1987; 60: 804–814
Morkin E, Bahl JJ, Markham BE: Control of cardiac myosin heavy chain gene expression by thyroid hormone, in: Cellular and Molecular Biology of Muscle Development. New York, Alan R Liss Inc, 1989, pp 381–389
Zierhut W, Zimmer HG: Triiodothyronine-induced changes in function, metabolism and weight of the rat heart: Effects of alpha-and beta-adrenergic blockade. Basic Res Cardiol 1989; 84: 359–370
Klein I, Hong C: Effects of thyroid hormone on cardiac size and myosin content of the heterotopically transplanted rat heart. J Clin Invest 1986; 77: 1694–1698
Korecky B, Zak R, Schwartz K, Aschenbrenner V: Role of thyroid hormone in regulation of isomyosin composition, contractility, and size of heterotopically isotransplanted rat heart. Circ Res 1987; 60: 824–830
Crie JS, Wakeland JR, Mayhew BA, Wildenthal K: Direct anabolic effects of thyroid hormone on isolated mouse heart. Am J Physiol 1983; 245: C328 - C333
Lompre AM, Schwartz K, d’Albis A, Lacombe G, van Thiem N, Swynghedauw B: Myosin isoenzyme redistribution in chronic heart overload. Nature 1979; 282: 105–107
Friberg P, Rupp H, Nordlander M: Functional and biochemical analyses of isolated hearts in renal and reversed renal hypertension. Acta Physiol Scand 1989; 135: 123–132
Pauletto P, Vescovo G, Scannapieco G, Angelini A, Pessina AC, Dalla Libera L, Carraro U, Dal Palu C: Changes in rat ventricular isomyosins with regression of cardiac hypertrophy. Hypertension 1986; 8: 1143–1148
Dussaule JC, Michel JB, Auzan C, Schwartz K, Corvol P, Menard J: Effect of antihypertensive treatment on the left ventricular isomyosin profile in one-clip, two kidney hypertensive rats. J Pharmacol Exp Ther 1986; 236: 512–518
Sen S, Young DR: Role of sodium in modulation of myocardial hypertrophy in renal hypertensive rats. Hypertension 1986; 8: 918–924
Xenophontos XP, Watson PA, Chua BHL, Haneda T, Morgan HE: Increased cyclic AMP content accelerates protein synthesis in rat heart. Circ Res 1989; 65: 647–656
Lansman JB, Hallam TJ, Rink TJ: Single stretch-activated ion channels in vascular endothelial cells as mechanotransducers. Nature 1987; 325: 811–813
Izumo S, Nadal-Ginard B, Mandavi V: Protooncogene induction and reprogramming of cardiac gene expression produced by pressure overload. Proc Nat/ Acad Sci 1988; 85: 339–343
Simpson PC: Proto-oncogenes and cardiac hypertrophy. Annu Rev Physiol 1989; 51: 189–201
Martin AF, Robinson DC, Dowell RT: Isomyosin and thyroid hormone levels in pressure-overloaded weanling and adult rat hearts. Am J Physiol 1985; 248: H305 - H310
Izumo S, Lompre AM, Matsuoka R, Koren G, Schwartz K, Nadal-Ginard B, Mandavi V: Myosin heavy chain messenger RNA and protein isoform transitions during cardiac hypertrophy: Interaction between hemodynamic and thyroid hormone-induced signals. J Clin Invest 1987; 79: 970–977
Rupp H, Popova N, Jacob R: Dissociation between factors resulting in hypertrophy and changes in myosin isoenzyme population of the pressure-loaded heart, in Jacob R, Gulch R, Kissling G (eds): Cardiac Adaptation to Hemodynamic Overload, Training and Stress. Darmstadt, Steinkopff Verlag, 1983, pp 46–52.
Martin AF, Paul RJ, McMahon EG: Isomyosin transitions in ventricles of aldosterone-salt hypertensive rats. Hypertension 1986; 8: 128–132
Rupp H, Felbier HR, Bukhari AR, Jacob R: Modulation of myosin isoenzyme populations and activities of monoamine oxidase and phenylethanolamine-N-methyltransferase in pressure loaded and normal rat heart by swimming exercise and stress arising from electrostimulation in pairs. Can J Physiol Pharmacol 1984; 62: 1209–1218
Rupp H: Differential effect of physical exercise routines on ventricular myosin and peripheral catecholamine stores in normotensive and spontaneously hypertensive rats. Circ Res 1989; 65: 370–377
Rupp H: The adaptive changes in the isoenzyme pattern of myosin from hypertrophied rat myocardium as a result of pressure overload and physical training. Basic Res Cardiol 1981; 76: 79–88
Scheuer J, Malhotra A, Hirsch C, Capasso J, Schaible TF: Physiologic cardiac hypertrophy corrects contractile protein abnormalities associated with pathologic hypertrophy in rats. J Clin Invest 1982; 70: 1300–1305
Nagano M: Cardiac regression of spontaneously hypertensive rats treated with hypotensive drugs, in Papp JG: Cardiovascular Pharmacology ‘87. Budapest, Akademiai Kiado, pp 315–322, 1987
Rupp H, Berger HJ, Werdan K: Agents known to increase intracellular Ca2+ can redirect myosin heavy chain (HC) expression in favour of alpha-HC. Z Kardiol 1989; 78 (suppl 1): P105
Sen S, Tarazi RC: Regression of myocardial hypertrophy and influence of adrenergic system. Am J Physiol 1983; 244: H97 - H101
Rupp H, Jacob R: Correlation between total catecholamine content and redistribution of myosin isoenzymes in pressure loaded ventricular myocardium of the spontaneously hypertensive rat. Basic Res Cardiol 1985; 81 (suppl 1): 147–155.
Mercadier JJ, Lompre AM, Wisnewsky C, Samuel JL, Bercovici J, Swynghedauw B, Schwartz K: Myosin isoenzymic changes in several models of rat cardiac hypertrophy. Circ Res 1981; 49: 525–532
Takeda N, Ohkubo T, Hatanaka T, Takeda A, Nakamura I, Nagano M: Myocardial contractility and left ventricular myosin isoenzyme pattern in cardiac hypertrophy due to chronic volume overload. Basic Res Cardiol 1987; 82 (suppl 2): 215–221
Noma K, Brändle M, Jacob R: Evaluation of left ventricular function in an experimental model of congestive heart failure due to combined pressure and volume overload. Basic Res Cardiol 1988; 83: 58–64
Baldwin KM, Cooke DA, Cheadle WG: Time course adaptations in cardiac and skeletal muscle to different running programs. J Appl Physiol 1977; 42: 267–272
Shepherd RE, Gollnick PD: Oxygen uptake of rats at different work intensities. Pflügers Arch 1976; 362: 219–222
Jacob R, Vogt M, Rupp H: Physiological and pathological hypertrophy, in Dhalla NS, Singal PK, Beamish RE (eds): Pathophysiology of Heart Disease. Boston, Martinus Nijhoff Publishing, pp 39–56, 1987
Simpson P: Norepinephrine-stimulated hypertrophy of cultured rat myocardial cells is an alpha-drenergic response. J Clin Invest 1983; 72: 732–738
Sreter FA, Faris R, Balogh I, Somogyi E, Sotonyi P: Changes in myosin isozyme distribution induced by low doses of isoproterenol. Arch Int Pharmacodyn 1982; 260: 159–164
Rupp H, Bukhari AR, Jacob R: Regulation of cardiac myosin isoenzymes. The interrelationship with catecholamine metabolism (abstract). J Mol Cell Cardiol 1983; 15 (suppl 1): 317
Buttrick P, Malhotra A, Factor S, Geenen D, Scheuer J: Effects of chronic dobutamine administration on hearts of normal and hypertensive rats. Circ Res 1988; 63: 173–181
Rupp H, Elimban V, Dhalla NS: Sucrose feeding prevents changes in myosin isoenzymes and sarcoplasmic reticulum Ca2+ -pump ATPase in pressure-loaded rat heart. Biochem Biophys Res Commun 1988; 156: 917–923
Author information
Authors and Affiliations
Editor information
Rights and permissions
Copyright information
© 1990 Kluwer Academic Publishers
About this chapter
Cite this chapter
Rupp, H., Jacob, R., Dhalla, N.S. (1990). Signal Transduction in Myocardial Hypertrophy and Myosin Expression. In: Korecky, B., Dhalla, N.S. (eds) Subcellular Basis of Contractile Failure. Developments in Cardiovascular Medicine, vol 116. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1513-1_9
Download citation
DOI: https://doi.org/10.1007/978-1-4613-1513-1_9
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4612-8813-8
Online ISBN: 978-1-4613-1513-1
eBook Packages: Springer Book Archive