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Am J Physiol Heart Circ Physiol 292: H2138-H2143, 2007; doi:10.1152/ajpheart.00852.2006
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Prevention of concentric hypertrophy and diastolic impairment in aortic-banded rats treated with resveratrol

Danijel Juric,1 Peter Wojciechowski,1 Dipak K. Das,2 and Thomas Netticadan1

1Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Manitoba, Canada; and 2Cardiovascular Research Center, University of Connecticut School of Medicine, Farmington, Connecticut

Submitted 8 August 2006 ; accepted in final form 27 September 2006

This study was designed to examine the effects of the antioxidant resveratrol on cardiac structure and function in pressure overload (PO)-induced cardiac hypertrophy. Male Sprague-Dawley rats were subjected to sham operation and the aortic banding procedure. A subgroup of sham control and aortic-banded rats were treated with resveratrol for 2 wk after surgery. Echocardiographic analysis of cardiac structure and function along with Western blot analysis of endothelial nitric oxide synthase (eNOS), inducible nitric oxide synthase (iNOS), and redox factor-1 (ref-1) were performed in all groups after 4 wk of surgery. Banded rats showed significantly increased left ventricle-to-body weight ratio. Echocardiographic analysis showed that the interventricular septal wall thickness and left ventricular posterior wall thickness at systole and diastole were significantly increased in banded rats. Also, a significant increase in isovolumic relaxation time was observed in banded rats. Measured eNOS, iNOS, and ref-1 protein levels were significantly reduced in banded rats. Resveratrol treatment prevented the above changes in cardiac structure, function, and protein expression in banded rats. Aortic banding after 4 wk resulted in concentric remodeling and impaired contractile function due to PO on the heart. The 2-wk treatment with resveratrol was found to abolish PO-induced cardiac hypertrophy. Resveratrol may therefore be beneficial against PO-induced cardiac hypertrophy found in clinical settings of hypertension and aortic valve stenosis.

pressure overload; nitric oxide; redox factor-1



Address for reprint requests and other correspondence: D. K. Das, Cardiovascular Research Center Univ. of Connecticut School of Medicine, Farmington, CT 06030-1110 (e-mail: ddas{at}neuron.uchc.edu)




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