Vascular smooth muscle cell polyploidy and cardiomyocyte hypertrophy due to chronic NOS inhibition in vivo (original) (raw)

Devlin, Alison M., Brosnan, M. Julia, Graham, Delyth ORCID: https://orcid.org/0000-0002-7328-4708, Morton, James J., McPhaden, Allan R., McIntyre, Martin, Hamilton, Carlene A., Reid, John L. and Dominiczak, Anna F. ORCID: https://orcid.org/0000-0003-4913-3608(1998) Vascular smooth muscle cell polyploidy and cardiomyocyte hypertrophy due to chronic NOS inhibition in vivo.American Journal of Physiology: Heart and Circulatory Physiology, 274(1), H52-H59. (PMID:9458851)

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Publisher's URL: http://ajpheart.physiology.org/content/274/1/H52

Abstract

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 withN G-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) fromL-NAME-treated WKY had a significantly higher polyploid population compared with WKY controls. Using organ bath experiments, we have shown that aortic rings fromL-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 thatL-NAME treatment caused reexpression of the fetal skeletal α-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.

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