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Am J Physiol Heart Circ Physiol 276: H350-H358, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 2, H350-H358, February 1999

Hypertrophic response to hemodynamic overload: role of load vs. renin-angiotensin system activation

Masaaki Koide1, Blase A. Carabello1, Chester C. Conrad2, John M. Buckley1, Gilberto DeFreyte1, Mary Barnes1, Robert J. Tomanek3, Chih-Chang Wei4, Louis J. Dell'Italia4, George Cooper IV1, and Michael R. Zile1

1 Cardiology Section of the Department of Medicine and the Department of Physiology, Gazes Cardiac Research Institute, Medical University of South Carolina and the Veterans Affairs Medical Center, Charleston, South Carolina 29401; 2 Veterans Affairs Medical Center, Boston, Massachusetts 02130; 3 Department of Anatomy and Cell Biology, University of Iowa College of Medicine, Iowa City, Iowa 52242; and 4 Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama 35294

Myocardial hypertrophy is one of the basic mechanisms by which the heart compensates for hemodynamic overload. The mechanisms by which hemodynamic overload is transduced by the cardiac muscle cell and translated into cardiac hypertrophy are not completely understood. Candidates include activation of the renin-angiotensin system (RAS) and angiotensin II receptor (AT1) stimulation. In this study, we tested the hypothesis that load, independent of the RAS, is sufficient to stimulate cardiac growth. Four groups of cats were studied: 14 normal controls, 20 pulmonary artery-banded (PAB) cats, 7 PAB cats in whom the AT1 was concomitantly and continuously blocked with losartan, and 8 PAB cats in whom the angiotensin-converting enzyme (ACE) was concomitantly and continuously blocked with captopril. Losartan cats had at least a one-log order increase in the ED50 of the blood pressure response to angiotensin II infusion. Right ventricular (RV) hypertrophy was assessed using the RV mass-to-body weight ratio and ventricular cardiocyte size. RV hemodynamic overload was assessed by measuring RV systolic and diastolic pressures. Neither the extent of RV pressure overload nor RV hypertrophy that resulted from PAB was affected by AT1 blockade with losartan or ACE inhibition with captopril. RV systolic pressure was increased from 21 ± 3 mmHg in normals to 68 ± 4 mmHg in PAB, 65 ± 5 mmHg in PAB plus losartan and 62 ± 3 mmHg in PAB plus captopril. RV-to-body weight ratio increased from 0.52 ± 0.04 g/kg in normals to 1.11 ± 0.06 g/kg in PAB, 1.06 ± 0.06 g/kg in PAB plus losartan and 1.06 ± 0.06 g/kg in PAB plus captopril. Thus 1) pharmacological modulation of the RAS with losartan and captopril did not change the extent of the hemodynamic overload or the hypertrophic response induced by PAB; 2) neither RAS activation nor angiotensin II receptor stimulation is an obligatory and necessary component of the signaling pathway that acts as an intermediary coupling load to the hypertrophic response; and 3) load, independent of the RAS, is capable of stimulating cardiac growth.

myocardial hypertrophy; angiotensin II; pulmonary artery band


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