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See article by Martin et al. [5] (pages 46–55) in this issue. The seminal observation by Furchgott and Zawadzki [1] of a paradoxical vasoconstrictive effect of acetylcholine in arteries deprived of endothelium paved the way for the rapid discovery of nitric oxide (NO) and of the mechanisms of NO generation by a specific family of isoforms known as NO synthases (NOS). The role of NO in the endothelium was characterized as a predominant mechanism of vasodilation through the production of cyclic GMP (cGMP) in vascular smooth muscle cells. The rapid progress of this research in endothelial cells automatically led to the question whether the cardiac cell itself could be a source of NO.It was found that the three characterized isoforms of NOS are expressed in cardiac myocytes [2]. However, the role of NO in the myocardium, and the regulation of its production, seems much more complex than what was described before in the endothelium, and includes both cGMP-dependent and -independent mechanisms. Myocardial NO is involved in cellular processes as diverse as cardiac contractility, Ca2+ handling, mitochondrial respiration, substrate metabolism, generation of radical oxygen species, and ischemic preconditioning among others (see Fig. 1). In addition, the mechanisms of action of NO are diverse and sometimes contradictory. For example, depending on the experimental setting, blocking cardiac NOS can be either beneficial or deleterious for the ischemic heart [3,4]. Part of this complexity comes from the fact that NO production in the heart is performed by the three different isoforms (endothelial, inducible and neuronal) that differ in their properties, … *Corresponding author. Tel.: +1 973 972 3926; fax: +1 973 972 7489. Email address: deprech{at}umdnj.edu

NO with no NOS in ischemic heart