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Cardiovascular Research 2005 66(3):421-422; doi:10.1016/j.cardiores.2005.03.022
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Copyright © 2005, European Society of Cardiology

Divergent roles of endothelial nitric oxide synthase in cardiac hypertrophy and chamber dilatation?

Ajay M. Shah

Department of Cardiology, GKT School of Medicine, King's College London, Bessemer Road, London SE5 9PJ, UK

Received 31 March 2005;
The first 10% of the full text of this article appears below.

See also article by Ruetten et al. [11] (pages 444–453) in this issue.

Nitric oxide (NO) influences many aspects of cardiac function including excitation–contraction coupling, myofilament function, oxygen consumption, substrate metabolism, and cell growth and survival [1,2]. All three NO synthase (NOS) isoforms, namely eNOS, nNOS, and iNOS, can be expressed in the heart. An important paradigm with respect to the cardiomyocyte has been the demonstration that eNOS and nNOS are both expressed in this cell type but have distinct effects on contractile function as a result of their specific subcellular localization and distinct interactions with and/or proximity to other . . . [Full Text of this Article]


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