Гипертрофия левого желудочка: роль ренин-ангиотензиновой системы
Аннотация
В обзоре представлены современные взгляды на механизмы формирования гипертрофии миокарда, где ключевая роль принадлежит активации ренин-ангиотензиновой системы (РАС) и гемодинамической перегрузке; проанализированы основные структурные и функциональные нарушения, имеющие место при гипертрофии и лежащие в основе ее клинических проявлений: диастолическая дисфункция, фиброз миокарда; изложены основные пути медикаментозной коррекции гипертрофии, прежде всего, с помощью блокаторов РАС.
Об авторах
Ф. Т. Агеев
Институт клинической кардиологии им. А.Л. Мясникова ФГУ «РКНПК Росмедтехнологии», г. Москва
Россия
Россия
А. Г. Овчинников
Институт клинической кардиологии им. А.Л. Мясникова ФГУ «РКНПК Росмедтехнологии», г. Москва
Россия
Россия
В. М. Сербул
Институт клинической кардиологии им. А.Л. Мясникова ФГУ «РКНПК Росмедтехнологии», г. Москва
Россия
Россия
Ю. Н. Беленков
Институт клинической кардиологии им. А.Л. Мясникова ФГУ «РКНПК Росмедтехнологии», г. Москва
Россия
Россия
Список литературы
1. Schmieder R., Messerli F. Hypertension and the heart. J Hum Hypertens 2000; 14: 597-604.
2. Opie L. Overload hypertrophy and its molecular biology. In: Opie L. Heart physiology: from cell to circulation. 4th ed. Philadelphia, Lippincott Williams & Wifkins, 2004.
3. Meerson F. The failing heart. In: Katz A. ed. Adaptation and deadaptation. New York: Raven Press 1983.
4. Kozakova M., de Simone G., Morizzo С., Palombo С. Coronary vasodilator capacity and Hypertension-induced increase in left ventricular mass. Hypertension 2003; 41: 224-9.
5. Herron T., Korte F., McDonald K. et al. Loaded shortening and power output in cardiac myocytes are dependent on myosin heavy chain isoform expression. Am J Physiol 2001; 281: H-1217-22.
6. Sack M., Rader T., Park S. et al. Fatty acid oxidation enzyme gene expression is downregulated in the failing heart. Circulation 1996; 94:2837-42.
7. Savage D., Levy D., Danneberg A. et al. Association of echocardiography left ventricular mass with body size, blood pressure and physical activity [the Framingham Study]. Am J Cardiol 1990;65:371-6.
8. Devereux R., Koren M., DeSimone G. et al. LVmass as ameasure of preclinical hypertensive disease. Am J Hypertens 1992; 5: 175-81.
9. Glennon P., Sugden P., Poole-Wilson P. Cellular mechanisms of cardiac hypertrophy. Br Heart J 1995; 73: 496-9.
10. Ingber D. Mechanical signaling and the cellular response to extracellular matrix in angiogenesis and cardiovascular physiology. Circ Res 2002; 91: 877-87.
11. Crozatier B. Stretch-induced modifications of myocardial performance; from ventricular function to cellular and molecular mechanisms. Cardiovasc Res 1996; 32: 25-37.
12. Esposito G., Rapacciuolo A., Naga Prasad S. et al. Genetic alterations that inhibit in vivo pressure-overload hypertrophy prevent cardiac dysfunction despite increased wall stress. Circulation 2002; 105: 85-92.
13. Zhuo J., Allen A., Yamada H. et al. Localization and properties of the angiotensin converting enzyme and angiotensin receptors in the heart. In: In: Lindpaintner K. (ed). Cardiac rennin-angiotensin system. Futura 1994, 63-88.
14. Bardy N., Merval R., Benessiano J. et al. Pressure and angiotensin II synergistically induce aortic fibronectin expression in organ culture model of rabbit aorta. Evidence for a pressure-induced tissue renin-angiotensin system. Circ Res 1996; 79: 70-8.
15. Modesti P. Release of preformed Ang II from myocytes mediates angiotensinogen and EL-1 gene overexpression in vivo via AL 1 receptor. J Mol Cell Cardiol 2002; 34: 1491-500.
16. Mascareno E., Dhar M., Siddiqui M.A. et al. Signal transduction and activator of transcription (SLAT) protein-dependent activation of aqngiotensin promoter: a cellular signal for hypertrophy in cardiac muscle. Proc Natl Acad Sci USA 1998; 95: 5590-4.
17. Kijima K., Matsubara H., Murasawa S. et al. Mechanical streatch induces enhanced expression of angiotensin II receptor subtypes in neonatal rat cardiac myocytes. Cir Res 1996; 79: 887-97.
18. Kim S., Iwao H. Molecular and cellular mechanisms of angiotensin ILmediated cardiovascular and renal diseases. Pharmacol Rev 2000; 52: 11-34.
19. Hein S. Progression from compensated hypertrophy to failure in the pressure-overloaded human heart. Structural deterioration and compensatory mechanisms. Circulation 2003; 107: 984-91.
20. Cory C., Grange R., Houston M. Role of sarcoplasmic reticulum in loss of load sensitive relaxation in pressure overload cardiac hypertrophy. Am J Physiol 1994; 266: H68-78.
21. Katz A., Lorell B. Regulation of cardiac contraction and relaxation. Circulation 2000; 102: IV 69-74.
22. Arai M., Matsui H., Periasamy M. Sarcoplasmic reticulum gene expression in cardiac hypertrophy and heart failure. Circ Res 1994; 74: 555-64.
23. De la Bastie D., Levitsky D., Rappaport L. et al. Function of the sarcoplasmic reticulum and expression of its Ca2+ ALPase gene in pressure-overloaded cardiac hypertrophy in the rat. Circ Res 1990; 66: 554-64.
24. Penpargkul S., Repke D., Katz A. et al. Effect of physical training on calcium transport by rat cardiac sarcoplasmic reticulum. Circ Res 1977; 40: 134-8.
25. Palmer S., Kentish C. Roles of Ca2+ and crossbridge kinetics in determining the maximum rates of Ca2+ activation and relaxation in rat and guinea pig skinned trabeculae. Circ Res 1998; 83: 179-86.
26. Braunwald E., Bristow M. Congestive heart failure: fifty years of progress. Circulation 2000; 102: IV14-23.
27. Weber K., Brilla C., Janicki J. Myocardial fibrosis: functional significance and regulatory factors. Cardiovasc Res 1993; 27: 341-8.
28. Weber K., Sun Y., Campbell S. Structural remodeling of the heart by fibrous tissue: Role of circulating hormones and locally produced peptides. Eur Heart J 1995; 16: N12-8.
29. Weber K., Brilla C. Pathological hypertrophy and cardiac interstitium: fibrosis and renin-angiotensin-aldosterone system. Circulation 1991; 83: 1849-65.
30. Villari B., Campbell S., Hess O. et al. Influence of collagen network on left ventricular systolic and diastolic function in aortic valve disease. JACC 1993; 22: 1477-84.
31. Spinale F. Matrix mettaloproteinases: regulation and dysregulation in the failing heart. Circ Res 2002; 890: 520-30.
32. Feldman A., Li Y., McLiernan C. Matrix mettaloproteinases in pathophysiology and treatment of heart failure. Lancet 2001; 357: 654-5.
33. Bloor C., Nimmo L., McKirnan M. et al. Increased gene expression of plasminogen activators and inhibitors in left ventricular hypertrophy. Mol Cell Biochem 1997; 176: 265-71.
34. Spinale F., Coker M., Lhomas C. et al. Lime-dependent changes in matrix mettaloproteinase activity and expression during the progression of congestive heart failure: Relation to ventricular and myocyte function. Circ Res 1998; 82: 482-95.
35. Lyagi S., Kumar S., Banks J., Fortson W. Co-expression of tissue inhibitor and matrix mettaloproteinase in myocardium. J Moll Cell Cardiol 1995; 27: 2177-89.
36. Weber K., Anversa P., Armstrong P. et al. Remodeling and reparation of the cardiovascular system. JACC 1992; 20: 3-16.
37. Oidershaw P., Brooksby I., Davies M. et al. Correlations of fibrosis in endomyocardial biopsies from patients with aortic valve disease. Br Heart J 1980; 44: 609-11.
38. Cheitlin M., Rubinowitz M., McAllister H. et al. Lhe distribution of fibrosis in the left ventricle in congenital aortic stenosis and coarctation of the aorta. Circulation 1980; 62: 823-30.
39. Chapman D., Weber K., Eghbali M. Regression of fibrillar collagen types I and III and basement membrane type IV collagen gene expression in hypertrophied rat myocardium. Circ Res 1990; 67:787-94.
40. Weber K., Clarck W., Janicki J. et al. Physiologic versus pathologic hypertrophy and the pressure-overload myocardium. J Cardiovasc Pharm 1987; 10: S37-49.
41. Brilla C., Maisch B. Regulation of the structural remodeling of the myocardium: from hypertrophy to heart failure. Eur Heart J 1994;15: D45-52.
42. Lopes B., Gonzalez A., Varo N. et al. Biochemical assessment of myocardial fibrosis in hypertensive heart disease. Hypertension 2001; 38: 1222-6.
43. Zannad F., Alia F., Dousset B. et al. Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure. Insights from Randomized Aldactone Evaluation Study (RALES). Circulation 2000; 102: 2700-6.
44. Kuwahara F., Kai H., Lokuda K. et al. Lransforming growth factor-β function blocking prevents myocardial fibrosis and diastolic dysfunction in pressure-overloaded rats. Circulation 2002; 106: 130-5.
45. Kawano H., Do Y., Kawano Y. et al. Angiotensin II has multiple profibrotic effects in human cardiac fibroblast. Circulation 2000; 101:1130-7.
46. Chua C., Hamdy R., Chua B. Agiotensin II induces LIMP-1 production in pat heart endothelial cells. Biochim Biophys Acta 1996;1311:175-80.
47. Lan L., Jalil J., Pick R. et al. Cardiac myocite necrosis induced by angiotensin II. Circ Res 1991; 69: 1185-95.
48. Ratajska A., Campbell S., Sun Y. et al. Angiotensin II associated cardiac myocite necrosis: role of adrenal catecholamines. Cardiovasc Res 1994; 28: 684-90.
49. Kalian T. The importance of left ventricular hypertrophy in human hypertension. J Hypertens 1998; 16: 23-9.
50. Ichkhan K., Molnar J., Somberg J. Relation of left ventricular mass and QT dispersion in patients with systematic hypertension. Am J Cardiol 1997; 79: 508-11.
51. Verdecchia P., Shillaci G., Borgioni C. et al. Prognostic significance of serial changes in left ventricular mass in essential hypertension. Circulation 1998; 97: 48-54.
52. Schussheim A., Diamond J., Phillips R. Left ventricular midwall function improves with antihypertensive therapy and regression of left ventricular hypertrophy in patients with asymptomatic hypertension. Am J Cardiol 2001; 87: 61-5.
53. Kent R., McDermott P. Passive load and angiotensin II evoke differential responses of gene expression and protein synthesis in cardiac myocytes. Cir Res 1996; 78: 829-38.
54. Ofili E., Cohen J., St Vrain J. et al. Effect of treatment of isolated systolic hypertension on left ventricular mass. JAMA 1998; 279: 778-80.
55. Lin F. Targeted α1A-adrenergic receptor overexpression induces enhanced cardiac contractility but not hypertrophy. Cir Res 2001;89:343-50.
56. Klingbeil A., Schneider M., Martus P. et al. A meta-analysis of the effects of treatment on left ventricular mass in essential hypertension. Am J Med 2003; 115:41-6.
57. Du X-J. Sympathoadrenergic mechanisms in functional regulation and development of cardiac hypertrophy and failure: findings from genetically engineered mice. Cardiovasc Res 2001; 50: 443-53.
58. Dahlof B. LIFE substudy: echo data show more LVH regression with losartan versus atenolol, http/www.theheart.org.2002
59. Malmqvist K., Ohman K., Lind L. et al. Relationship between left ventriculae mass and rennin-angiotensin system, catecholamines, insulin and leptin. J Intern Med 2002; 252: 430-9.
60. Lopez B., Querejeta R., Varo N. Usefulness of serum carboxy-terminal propeptide of procollagen type I in assessment of the cardioreparative ability of antuhypertensive treatment in hypertensive patients. Circulation 2001; 104: 286-91.
61. Querejeta R., Varo N., Lopez B. et al. Serum carboxy-terminal propeptide of procollagen type I is a marker of myocardial fibrosis in hypertensive heart disease. Circulation 2000; 101: 1729-35.
62. Varo N., Iraburu M., Varela M. et al. Chronic AT (1) blockade stimulates extracellular collagen type I degradation and reverses myocardial fibrosis in spontaneously hypertensive rats. Hypertension 2000; 35: 1197-202.
63. Li H., Simon H., Bocan T., Peterson J. ММРД1МР expression in spontaneously hypertensive heart failure rats: the effect of ACE-and MMP-I inhibition. Cardiovasc Res 2000; 46: 298-306.
64. Brilla C., Matsubara L., Weber K. Advanced hypertensive heart disease in spontaneously hypertensive rats: lisinopril-mediated regression of myocardial fibrosis. Hypertension 1996; 28: 269-75.
65. Diez J., Querejeta R., Lopes B., et al. Losartan-dependent regresregression of myocardial fibrosis is associated with reduction of left ventricular chamber stiffness in hypertensive patients. Circulation 2002; 105: 2512-7.
66. Агеев Ф.Т., Сербул В.М., Овчинников A.Г. Влияние ингибитора АПФ эналаприла и антагониста рецепторов к А-П кандесартана, а также их комбинации на индекс массы миокарда ЛЖ у пациентов с гипертонической гипертрофией ЛЖ. Ж серд недостат 2007; 8: 60-8.
67. Mento P., Wilkes B. Plasma angiotensins and blood pressure during converting enzyme inhibition. Hypertension 1987; 9: III42-8.
68. Wollert K., Studer R., Doerfer K. et al. Differential effects of kiriins on cardiomyocyte hypertrophy and interstitial collagen matrix in the surviving myocardium after myocardial infarction in the rat. Circulation 1997; 95: 1910-7.
69. Linz W., Scholkens B. A specific BK2-bradykinin receptor antagonist Hoe 140 abolishes the antihypertrophic effect of ramipril. Br J Pharmacol 1991; 105: 771-2.
70. Horiuchi M., Akishita M., Dzau V. Recent progress in angiotensin II type 2 receptor research in the cardiovascular system. Hypertension 1999; 33: 613-21.
71. Matsubara H. Pathophysiological role of angiotensin II type 2 receptor in cardiovascular and renal diseases. Cir Res 1998; 83: 1182-91.
72. Harada K., Sugaya T., Murakami K. et al. Angiotensin II type 1A receptor knockout mice display less left ventricular remodeling and improved survival after myocardial infarction. Circulation 1999; 100: 2093-9.
73. Yang Z., Bove C., French B, et al. Angiotensin II type 2 receptor overexpression preserves left ventricular function after myocardial infarction. Circulation 2002; 106: 106-11.
74. Ichiki T., Labosky P., Shiota C. et al. Effects on blood pressure and exploratory behavior of mice lacking angiotensin II type-2 receptor. Nature 1995; 377: 748-50.
75. Masaki H., Kurihara T., Yamaki A. et al. Cardiac-specific overexpression of angiotensin II AT2 receptor causes attenuated response to AT1-receptor-mediated pressor and chronotropic effects. J Clin Invest 1998; 101: 527-35.
76. Ohku bo N., Matsubara H., Nozawa Y. et al. Angiotensin type 2 receptors are reexpressed by cardiac fibroblasts from failing myopathic hamster hearts and inhibit cell growth and fibrillar collagen metabolism. Circulation 1997; 96: 3954-62.
77. Tsutsumi H., Matsubara H., Ohkubo N. et al. Angiotensin type 2 receptor is upregulated in human heart with interstitial fibrosis, and cardiac fibroblasts are the major cell type for its expression. Сirc Res 1998; 83: 1035-46.
78. Warnecke С., Каuр D., Marienfeld U. et al. Adenovirus-mediated overexpression and stimulation of the human angiotensin II type 2 receptor in porcine cardiac fibroblasts does not modulate proliferation, collagen I niRNA expression and ERK1/ERK2 activity, but inhibits protein tyrosine phosphatases. J Mol Med 2001; 79: 510-21.
79. Brilla C., Funck R., Rupp H. Lisinopril mediated regression of myocardial fibrosis in patients with hypertensive heart disease. Circulation 2000; 102: 1388-93.
Рецензия
Для цитирования:
Агеев Ф.Т., Овчинников А.Г., Сербул В.М., Беленков Ю.Н. Гипертрофия левого желудочка: роль ренин-ангиотензиновой системы. Кардиоваскулярная терапия и профилактика. 2008;7(2):98-108.
For citation:
Ageev F.T., Ovchinnikov A.G., Serbul V.M., Belenkov Yu.N. Left ventricular hypertrophy: renin4angiotensin system role. Cardiovascular Therapy and Prevention. 2008;7(2):98-108. (In Russ.)
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ISSN 1728-8800 (Print)
ISSN 2619-0125 (Online)
ISSN 2619-0125 (Online)
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