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Journal of Cardiovascular Pharmacology and Therapeutics
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1074248408320006v1
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*Compound via MeSH
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*Cardiomyopathy
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*CARVEDILOL
*ENALAPRIL MALEATE
*LOSARTAN POTASSIUM
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Enalapril and Losartan Are More Effective Than Carvedilol in Preventing Dilated Cardiomyopathy in the Syrian Cardiomyopathic Hamster

Maria J. Crespo, PhD

Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico, mcrespo{at}rcm.upr.edu

Nildris Cruz, MS

Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico

Pablo I. Altieri, MD

Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico

Nelson Escobales, PhD

Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico

To assess the role of the renin—angiotensin (RAS) and adrenergic systems in the development and progression of dilated cardiomyopathy in the Syrian cardiomyopathic hamster (SCH), echocardiographic parameters were evaluated in 6-month-old animals after 5 months of treatment with enalapril (25 mg/kg/day) plus losartan (10 mg/kg/day), or with carvedilol (1 mg/kg/day). Cardiac output indexes (COI) increased by 53% after RAS blockade and by 20% after β-blockade in SCH. Moreover, LVEDV and LVESV decreased 30% and 62%, respectively (P < .05) during RAS blockade, whereas ejection fraction (EF) increased by 48%. By contrast, carvedilol reduced LVESV by only 28% (P < .05) and increased EF by only 15% (P < .05). These results suggest that RAS activation plays a critical role in the development of cardiac dysfunction in SCH and that suppression of RAS may be more effective than β-blockade in retarding the development of cardiomyopathy in SCH. Owing to timing (pre—heart failure stage) and to the single dose protocol, the implications of this study for human subjects remain to be clarified.

Key Words: heart failure • enalapril • losartan • carvedilol • Syrian cardiomyopathic hamsters • cardiac function • dilated cardiomyopathy

This version was published on September 1, 2008

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 13, No. 3, 199-206 (2008)
DOI: 10.1177/1074248408320006


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