Nitric Oxide Determinations: Much Ado About N[O.Sup.*]-Thing?(Editorial‪)‬

The nitric oxide radical (N[O.sup.*]) is an important mediator of both physiological and pathophysiological processes. N[O.sup.*] is produced by nitric oxide synthase (NOS; EC 1.14.13.39), an enzyme that exists in three isoforms encoded by distinct genes [1, 2]. All isoforms of NOS catalyze the conversion of L-arginine into citrulline and N[O.sup.*]. In this reaction, which requires oxygen and NADPH, a guanidino-nitrogen atom of L-arginine is incorporated into N[O.sup.*]. Neuronal NOS (type I, nNOS) and endothelial (type III, eNOS) are [Ca.sup.2+]--and calmodulin-dependent constitutive NOS isoforms. nNOS has a function in neurotransmission. N[O.sup.*] produced by eNOS is identical to endothelium-derived relaxing factor and is the principal signal for relaxation of vascular smooth muscle cells. In addition, N[O.sup.*] produced by the endothelium has antithrombotic actions. Thus, eNOS and nNOS isoforms have important functions under normal conditions. They are present intracellularly, are rapidly activated by intracellular [Ca.sup.2+] fluxes, and produce small quantities of N[O.sup.*]. Inducible NOS (iNOS, type II) is not expressed under normal conditions.