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Am J Physiol Heart Circ Physiol 279: H2797-H2806, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 6, H2797-H2806, December 2000

Renin-angiotensin system and sympathetic nervous system in cardiac pressure-overload hypertrophy

Wendell S. Akers1, Andrew Cross2, Robert Speth3, Linda P. Dwoskin2, and Lisa A. Cassis2

Divisions of 1 Pharmacy Practice and Science and 2 Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, Kentucky 40536; and 3 Department of Veterinary Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman, Washington 99163

Angiotensin II and norepinephrine (NE) have been implicated in the neurohumoral response to pressure overload and the development of left ventricular hypertrophy. The purpose of this study was to determine the temporal sequence for activation of the renin-angiotensin and sympathetic nervous systems in the rat after 3-60 days of pressure overload induced by aortic constriction. Initially on pressure overload, there was transient activation of the systemic renin-angiotensin system coinciding with the appearance of left ventricular hypertrophy (day 3). At day 10, there was a marked increase in AT1 receptor density in the left ventricle, increased plasma NE concentration, and elevated cardiac epinephrine content. Moreover, the inotropic response to isoproterenol was reduced in the isolated, perfused heart at 10 days of pressure overload. The affinity of the beta 2-adrenergic receptor in the left ventricle was decreased at 60 days. Despite these alterations, there was no decline in resting left ventricular function, beta -adrenergic receptor density, or the relative distribution of beta 1- and beta 2-receptor sites in the left ventricle over 60 days of pressure overload. Thus activation of the renin-angiotensin system is an early response to pressure overload and may contribute to the initial development of cardiac hypertrophy and sympathetic activation in the compensated heart.

beta -adrenergic receptor; norepinephrine; heart failure; left ventricle


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