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Am J Physiol Heart Circ Physiol 274: H52-H59, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H52-H59, January 1998

Vascular smooth muscle cell polyploidy and cardiomyocyte hypertrophy due to chronic NOS inhibition in vivo

Alison M. Devlin1, M. Julia Brosnan1, Delyth Graham1, James J. Morton1, Allan R. McPhaden2, Martin McIntyre1, Carlene A. Hamilton1, John L. Reid1, and Anna F. Dominiczak1

Departments of 1 Medicine and Therapeutics and 2 Pathology, University of Glasgow, Western Infirmary, Glasgow G11 6NT, United Kingdom

To assess the vascular and cardiac response to NO (nitric oxide) synthase (NOS) blockade in vivo, Wistar-Kyoto rats (WKY) were treated for 3 wk with NG-nitro-L-arginine methyl ester (L-NAME; 10 mg · kg-1 · day-1). L-NAME treatment induced hypertension that was associated with increased plasma renin activity. Flow cytometry cell cycle DNA analysis showed that aortic vascular smooth muscle cells (VSMC) from L-NAME-treated WKY had a significantly higher polyploid population compared with WKY controls. Using organ bath experiments, we have shown that aortic rings from L-NAME-treated WKY have an increased contractile response to phenylephrine and impaired relaxation to carbachol compared with control rings. NOS blockade in vivo caused a significant increase in cardiac and left ventricular hypertrophy. Northern mRNA analysis of the myocardium showed that L-NAME treatment caused reexpression of the fetal skeletal alpha -actin isoform without alterations in collagen type I expression, a pattern indicating true hypertrophy of the cardiomyocytes. These studies provide further insight to confirm that NO deficiency in vivo results in the development of vascular and cardiac hypertrophy.

cell cycle; hypertension; renin-angiotensin system; NG-nitro-L-arginine methyl ester; skeletal alpha -actin


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