This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ruzicka, M. Articles by Leenen, F. H. Search for Related Content PubMed PubMed Citation Articles by Ruzicka, M. Articles by Leenen, F. H.

Circulation, Vol 90, 484-491, Copyright © 1994 by American Heart Association

ARTICLES

Effects of enalapril versus losartan on regression of volume overload- induced cardiac hypertrophy in rats

M Ruzicka, B Yuan and FH Leenen
Hypertension Unit, University of Ottawa Heart Institute, Ontario, Canada.

BACKGROUND: The role of nonhemodynamic cardiac trophic mechanisms differs not only between different models of cardiac hypertrophy but also within the same model for development versus maintenance of cardiac hypertrophy. Our previous studies pointed to a major role for the renin-angiotensin system (RAS) as a cardiac trophic stimulus in the remodeling of the heart in response to volume overload by aortocaval shunt or minoxidil treatment. METHODS AND RESULTS: In the present study, we evaluated the effects of blockade of the RAS by the angiotensin-converting enzyme inhibitor enalapril and the angiotensin II receptor blocker losartan on left ventricular (LV) and right ventricular mass and LV dilation in relation to changes in central hemodynamics during the maintenance of minoxidil and aortocaval shunt- induced cardiac hypertrophy. Both blockers similarly decreased LV end- diastolic pressure (LVEDP) and LV peak systolic pressure, whereas cardiac output remained unchanged in both models of volume overload. This suggests a major contribution of improved LV performance and decreased afterload to the decrease in cardiac preload by the two blockers rather than decreased venous return. Both blockers reversed LV hypertrophy in parallel to their effects on LVEDP in both models of volume overload. In minoxidil-treated rats, the extent of reversal in LV mass and dilation by the two blockers was similar to "spontaneous regression" after discontinuation of minoxidil treatment. CONCLUSIONS: These results indicate that in contrast to the development phase of cardiac hypertrophy, the RAS does not contribute to the maintenance of volume overload-induced cardiac hypertrophy in these two models via direct cardiac trophic effects. The RAS, however, maintains cardiac hypertrophy indirectly by contributing to the persistence of high filling pressures.

This article has been cited by other articles:

				L. M. D. Stefano, L. S. Matsubara, and B. B. Matsubara Myocardial dysfunction with increased ventricular compliance in volume overload hypertrophy Eur J Heart Fail, December 1, 2006; 8(8): 784 - 789. [Abstract] [Full Text] [PDF]

				X. Wang, E. Sentex, D. Chapman, and N. S. Dhalla Alterations of adenylyl cyclase and G proteins in aortocaval shunt-induced heart failure Am J Physiol Heart Circ Physiol, July 1, 2004; 287(1): H118 - H125. [Abstract] [Full Text] [PDF]

				P. A. Modesti, S. Vanni, I. Bertolozzi, I. Cecioni, C. Lumachi, A. M. Perna, M. Boddi, and G. F. Gensini Different Growth Factor Activation in the Right and Left Ventricles in Experimental Volume Overload Hypertension, January 1, 2004; 43(1): 101 - 108. [Abstract] [Full Text] [PDF]

				N C Sundgren, G D Giraud, P J S Stork, J G Maylie, and K L Thornburg Angiotensin II stimulates hyperplasia but not hypertrophy in immature ovine cardiomyocytes J. Physiol., May 1, 2003; 548(3): 881 - 891. [Abstract] [Full Text] [PDF]

				F. H. H. Leenen and B. Yuan Mortality After Coronary Artery Occlusion in Different Models of Cardiac Hypertrophy in Rats Hypertension, February 1, 2001; 37(2): 209 - 215. [Abstract] [Full Text] [PDF]

				S. Kim and H. Iwao Molecular and Cellular Mechanisms of Angiotensin II-Mediated Cardiovascular and Renal Diseases Pharmacol. Rev., March 1, 2000; 52(1): 11 - 34. [Abstract] [Full Text] [PDF]

				C. D. Thienelt, E. O. Weinberg, J. Bartunek, and B. H. Lorell Load-Induced Growth Responses in Isolated Adult Rat Hearts : Role of the AT1 Receptor Circulation, June 17, 1997; 95(12): 2677 - 2683. [Abstract] [Full Text]

				L. M. de Lannoy, A. H. J. Danser, J. P. van Kats, R. G. Schoemaker, P. R. Saxena, and M. A. D. H. Schalekamp Renin-Angiotensin System Components in the Interstitial Fluid of the Isolated Perfused Rat Heart : Local Production of Angiotensin I Hypertension, June 1, 1997; 29(6): 1240 - 1251. [Abstract] [Full Text]

				E. O. Weinberg, M. A. Lee, M. Weigner, K. Lindpaintner, S. P. Bishop, C. R. Benedict, K. K. L. Ho, P. S. Douglas, E. Chafizadeh, and B. H. Lorell Angiotensin AT1 Receptor Inhibition : Effects on Hypertrophic Remodeling and ACE Expression in Rats With Pressure-Overload Hypertrophy due to Ascending Aortic Stenosis Circulation, March 18, 1997; 95(6): 1592 - 1600. [Abstract] [Full Text]

				S. B. Harrap and J. B. O'Sullivan Cardiac Transplantation, Perindopril, and Left Ventricular Hypertrophy in Spontaneously Hypertensive Rats Hypertension, October 1, 1996; 28(4): 622 - 626. [Abstract] [Full Text]

				A. Calderone, N. Takahashi, N. J. Izzo Jr, C. M. Thaik, and W. S. Colucci Pressure- and Volume-Induced Left Ventricular Hypertrophies Are Associated With Distinct Myocyte Phenotypes and Differential Induction of Peptide Growth Factor mRNAs Circulation, November 1, 1995; 92(9): 2385 - 2390. [Abstract] [Full Text]

				M. Ruzicka and F. H. H. Leenen Relevance of Blockade of Cardiac and Circulatory Angiotensin-Converting Enzyme for the Prevention of Volume Overload–Induced Cardiac Hypertrophy Circulation, January 1, 1995; 91(1): 16 - 19. [Abstract] [Full Text]