AJP - Heart and Circulatory Physiology, Vol 264, Issue 6 2056-H2067, Copyright © 1993 by American Physiological Society

ARTICLES

Alterations in ANG II responsiveness in left and right myocardium after infarction-induced heart failure in rats

J. M. Capasso, P. Li, X. Zhang, L. G. Meggs and P. Anversa
Department of Medicine, New York Medical College, Valhalla, New York 10595.

To determine the effects of coronary arterial occlusion on the contractile response of the heart to angiotensin II (ANG II) administration, large infarcts were surgically induced in Sprague-Dawley rats at 2 mo of age. Forty-eight hours later, hearts from experimental animals presented a hemodynamic profile indicative of left ventricular failure and right ventricular dysfunction and revealed a loss of mass of 49.3 +/- 10.8% of the left ventricle inclusive of the interventricular septum. Plasma renin activity was found to be decreased by 48% in animals with occlusion of the left main coronary artery. Left and right posterior papillary muscles removed from these same hearts were evaluated mechanically in the presence and absence of ANG II. Contractile performance was impaired in left ventricular myocardium from infarcted rats as evidenced by the inability to attain developed tension similar to that seen in control rats. In addition, peak rates of tension rise and decay were significantly depressed. A reduction in contraction duration was also found in experimental animals, limiting the active state of the myocardium. ANG II resulted in a depression in the force-generating ability of left and right papillary muscles of control and experimental animals. Importantly, the negative inotropic effect of ANG II affected the left and right myocardium from infarcted rats by nearly twofold and threefold more than the corresponding muscles from controls. Morphometric evaluation revealed the absence of damage in both papillary muscles from control hearts and in the right muscles from experimental animals. However, necrotic tissue comprised 28.3 +/- 9.8% of left papillary muscles obtained from infarcted ventricles. It is concluded that ANG II administration resulted in reduced mechanical performance of rat myocardium. Coronary arterial ligation potentiated this phenomenon, and such a negative effect may have implication in infarction induced heart failure in vivo.

This article has been cited by other articles:

				J. Palomeque, L. Sapia, R. J. Hajjar, A. Mattiazzi, and M. Vila Petroff Angiotensin II-induced negative inotropy in rat ventricular myocytes: role of reactive oxygen species and p38 MAPK Am J Physiol Heart Circ Physiol, January 1, 2006; 290(1): H96 - H106. [Abstract] [Full Text] [PDF]

				D. Schultz, X. Su, C.-C. Wei, S. P. Bishop, P. Powell, G. H. Hankes, A. R. Dillon, P. Rynders, F. G. Spinale, G. Walcott, et al. Downregulation of ANG II receptor is associated with compensated pressure-overload hypertrophy in the young dog Am J Physiol Heart Circ Physiol, February 1, 2002; 282(2): H749 - H756. [Abstract] [Full Text] [PDF]

				M. C. G. Daniels, R. S. Keller, and P. P. de Tombe Losartan prevents contractile dysfunction in rat myocardium after left ventricular myocardial infarction Am J Physiol Heart Circ Physiol, November 1, 2001; 281(5): H2150 - H2158. [Abstract] [Full Text] [PDF]

				K. Harada, T. Sugaya, K. Murakami, Y. Yazaki, and I. Komuro Angiotensin II Type 1A Receptor Knockout Mice Display Less Left Ventricular Remodeling and Improved Survival After Myocardial Infarction Circulation, November 16, 1999; 100(20): 2093 - 2099. [Abstract] [Full Text] [PDF]

				G. Redaelli, A. Malhotra, B. Li, P. Li, E. H. Sonnenblick, P. A. Hofmann, and P. Anversa Effects of Constitutive Overexpression of Insulin-Like Growth Factor-1 on the Mechanical Characteristics and Molecular Properties of Ventricular Myocytes Circ. Res., March 23, 1998; 82(5): 594 - 603. [Abstract] [Full Text] [PDF]

				C.-P. Cheng, M. Suzuki, N. Ohte, M. Ohno, Z.-M. Wang, and W. C. Little Altered Ventricular and Myocyte Response to Angiotensin II in Pacing-Induced Heart Failure Circ. Res., May 1, 1996; 78(5): 880 - 892. [Abstract] [Full Text]