Devlin, A. M., Brosnan, M. J., Graham, D. , Morton, J. J., McPhaden, A. R., McIntyre, M., Hamilton, C. A., Reid, J. L. and Dominiczak, A. F. (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)
Full text not currently available from Enlighten.
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.
University Staff: Request a correction | Enlighten Editors: Update this record
Deposit and Record Details
Deposit and Record Details