Abstract
Nitric oxide was first considered to be a cardioprotective molecule from its action on the coronary circulation, because it dilates the vasculature and inhibits platelet/neutrophil activation. However, besides increasing cGMP production via the activation of guanylate cyclase, NO exerts a variety of actions. Some of them cause toxic effects on the cardiovascular system. It is widely recognized that NO reacts with superoxide and produces highly reactive peroxynitrate, which nitrosylates proteins. We demonstrated that NO produces an adduct with glutathione peroxidase, which is a key enzyme metabolizing the oxygen radical in the cytosol, and increases the sensitivity of myocytes to ischemia-reperfusion injury. Oxidative stress not only causes ischemiareperfusion injury of hearts, but also induces cellular injury in myocarditis, cardiomyopathy, and heart failure. Therefore, NO may also be involved in the pathogenesis of these cardiac diseases by modulating the redox state of the heart.
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© 2000 Springer-Verlag Tokyo
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Kuzuya, T., Nishida, M. (2000). Role of NO in Myocardial Injury Induced by Oxidative Stress: Ischemia, Myocarditis, Cardiomyopathy, and Heart Failure. In: Kitabatake, A., Sasayama, S., Francis, G.S., Okamoto, H. (eds) Heart Failure. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68331-5_7
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DOI: https://doi.org/10.1007/978-4-431-68331-5_7
Publisher Name: Springer, Tokyo
Print ISBN: 978-4-431-68333-9
Online ISBN: 978-4-431-68331-5
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