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) nitric oxide 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.
This brief review focuses on the role of NO in ischemic myocardial protection with emphasis on its contribution to ischemic pre-and post-conditioning cardioprotection. The impact of pathologic conditions on NO bioavailability and NO-signaling and its potential means for improvement, will also be discussed.
Keywords: Nitric oxide, cardiac ischemia, synthesized, endothelial, neuronal, cardioprotective, necrosis, myocardial, potential, tetrahydrobiopterin, reoxygenationinduced, atherosclerosis, PATHOGENESIS, exogenous, nitroglycerin
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