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Bentham Science Publishers, Current Pharmaceutical Design, 18(17), p. 1774-1782

DOI: 10.2174/138161211796391047

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Nitric Oxide and Protection against Cardiac Ischemia

Journal article published in 2011 by Zhengyuan Xia, Paul M. Vanhoutte
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Nitric oxide (NO) is produced in almost all tissues and it exerts a variety of biological actions under both physiological and pathological conditions. It is synthesized by three distinct enzymes: endothelial (eNOS), neuronal (nNOS) and inducible (iNOS) nitricoxide synthases. NO is a cardioprotective mediator in powerful cardioprotective processes such as pre- and post-conditioning ischemia;they operate largely in a NO-dependent manner. However, the activity of different NOSs isoforms as well as, the bioavailability of NO can be affected by a variety of disease conditions (in particular diabetes) and pathological situations associated with significantly elevated levels of the pro-inflammatory cytokine tumor necrosis factor-α (TNF-α). These adversely affect NO-signaling, as well as the efficacy and safety of treatments with NO or NO-containing agents.