“…Since the identification of nitric oxide (NO) as the endothelium‐derived relaxing factor, its role as secondary intra‐ and intercellular messenger in several physiological and pathophysiological conditions has been thoroughly investigated [1,2]. NO is physiologically produced by the catalysis of nitric oxide synthases (NOS), which are Ca 2+ ‐calmodulin (CaM)‐dependent enzymes [3]. There are three NOS isoforms, i NOS (inducible), n NOS (neuronal) and e NOS (endothelial), which are homodimeric, with each monomer containing an N‐terminal oxygenase and a C‐terminal reductase domain, connected by a CaM‐binding site [4].…”