Abstract
Nitric oxide is a key player among the numerous mediators of endothelial homeostasis and cardiac contractility and is thereby involved in the pathogenic processes leading to vascular and myocardial dysfunctions. Although none of the current paradigms would elevate the influence of NO on cardiac contraction to the level of that of e.g., catecholamines or increased calcium, this unusual signaling molecule can modulate virtually all the regulatory steps of excitationcontraction coupling and influence the course of cardiac decompensation. Not only alterations in spatial confinement or post-translational modifications but also changes in the abundance of one of the three NOS isoforms may result in profound cellular disturbancies that participate in the endothelial and contractile dysfunctions leading to cardiovascular diseases.
Keywords: nitric oxide, nitric oxide synthase, heart, endothelium, coronary, ischemia, Infarct, mechanoenergetic uncoupling
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