Abstract
Cardiac hypertrophy in rats was produced by aortic banding for 6 weeks and regression of hypertrophy in these experimental animals was induced by administration of angiotensin converting enzyme inhibitor, enalapril (10 mg/kg/ day) for 6 weeks. The left ventricular muscle mass and systolic pressure were decrease upon treating the hypertrophied rats with enalapril. This drug also decreased the number of α1-adrenoceptors in hypertrophyied myocardium without any changes in β-adrenoceptors. The regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril for 10 weeks was not associated with any alterations in α1-adrenoceptors in hypertrophied myocardium, but was decreased in β-adrenoceptors. Effects of enalapril on extracellular matrix in the myocardium was also observed in regression of hypertrophy in which the type III collagen mRNA expression and collagen contents were reduced in comparison with those of hypertrophied myocardium. These results indicate that regression of cardiac hypertrophy is not always associated with a decrease in the number of α1-adrenergic receptors and that the beneficial effects of enalapril in the hypertrophied heart in aortic banding animals may be of some specific nature. (Mol Cell Biochem 119: 23–28, 1993.
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References
Sen S: Regression of cardiac hypertrophy: experimental animal model. Am J Med 75 (suppl 3A): 87–93, 1983
Ganguly PK, Lee SL, Beamish RE, Dhalla NS: Altered sympathetic system and adrenoceptors during the development of cardiac hypertrophy. Am Heart J 118: 520–528, 1989
Sen S, Trazi RC: Regression of myocardial hypertrophy and influence of adrenergic system. Am J Physiol 244 (Heart Circ Physiol 13): H97–H101, 1983
Limas CJ: Increased number of β-adrenergic receptors in the hypertrophied myocardium. Biochem Biophy Acta 588:174–178, 1979
Limas CJ, Limas C: Reduced number of β-adrenergic receptors in the myocardium of spontaneously hypertensive rats. Biochem Biophys Res Commun 83: 710–714, 1978
Ayobe MH, Tarazi RC: Reversal of changes in myocardial β-receptors and inotropic responsiveness with regression of cardiac hypertrophy in renal hypertensive rat (RHR). Cir Res 54: 125–134, 1984
Kromer EP, Riegger GA: Effects of long-term angiotensin converting enzyme inhibition on myocardial hypertrophy in experimental aortic stenosis in the rat. Am J Cardiol 62: 161–163, 1988
Asmer RG, Dannier B, Santoni JPH, Laurent ST, London GM, Levy BI, Safar ME: Reversion of cardiac hypertrophy and reduced arterial compliance after converting enzyme inhibitor in essential hypertension. Cir Res 78: 941–950, 1988
Nakashima Y, Fouad FM, Tarazi RC: Regression of left ventricular hypertrophy from systemic hypertension by enalapril. Am J Cardiol 53: 1044–1049, 1984
Nakanishi H, Makino N, Hata T, Matsui H, Yano K, Yanaga T: Sarcolemmal Ca transport activities in cardiac hypertrophy caused by pressure overload. Am J Physiol 257 (Heart Circ Physiol 26): H349–H356, 1989
Lowry OH, Rosenbrough NJ, Farr AL, Randall RJ: Protein measurement with the Folin phenol reagent. J Biol Chem 193: 256–275, 1951
Snavely MD, Mahan LC, O’Connor T, Insel A: Selective down-regulation of adrenergic receptor subtypes in tissues from rats with pheochromocytoma. Endocrinology 113: 354–361, 1983
Corr PB, Crafford WA: Enhanced α-adrenergic responsiveness in the myocardium: Role of α-adrenergic blocker. Am Heart J 102: 605–614, 1981
Chirgwin JJ, Przbyla AE, MacDonald RJ, Rutter WJ: Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 18: 5294–5302, 1979
Thomas PS. Hybridization of denaturated RNA transferred or dotted to nitrocellulose paper. Method Enzymol 100: 255–266, 1983
Bergman J, Loxley R: Two improved and simplified methods for the spectrophotometric determination of hydroxyproline. Anal Chem 36: 1961–1965, 1963
Tamai J, Hori M, Kagiya T, Inoue M, Kamada T: Role of α1-adrenoceptor activity in progression of cardiac hypertrophy in guinea pig hearts with pressure overload. Cardiovasc Res 23: 315–322, 1989
Fox AW, Juberg EN, May JM, Johnson RD, Abel PW: Thyroid status and adrenergic receptor subtypes in the rat: Compari son of receptor density and responsiveness. J Pharmacol Exp Therap 235: 715–723, 1985
William LT, Lefkowitz RJ, Watanabe AM, Hathaway KR, Besch HR Jr: Thyroid hormone regulation of α-adrenergic receptor number. J Biol Chem 252: 2787–2789, 1977
Weber KT: Cardiac interstitum in health and disease: the fibrillar collagen network. J Am Coll Cardiol 13: 1639–1952
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© 1993 Springer Science+Business Media Dordrecht
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Makino, N., Matsui, H., Masutomo, K., Hata, T., Yanaga, T. (1993). Effect of Angiotensin Coverting Enzyme Inhibitor on Regression in Cardiac Hypertrophy. In: Yazaki, Y., Mochizuki, S. (eds) Cellular Function and Metabolism. Developments in Molecular and Cellular Biochemistry, vol 9. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3078-7_4
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DOI: https://doi.org/10.1007/978-1-4615-3078-7_4
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