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Nitric oxide (NO) is a highly diffusible, free radical signaling molecule that is produced by the endothelial NO synthase (eNOS) enzyme, which converts l-arginine and molecular oxygen into l-citrulline and NO.1,2 NO diffuses from the endothelium to the smooth muscle where it binds with high affinity to the heme group of soluble guanylate cyclase, which in turn catalyzes the conversion of GTP to cGMP.3 NO signaling is largely paracrine, with potential endocrine effects limited by its radical nature and extremely high reactivity with other heme-containing proteins such as hemoglobin and myoglobin.4 When NO encounters oxyhemoglobin in blood or oxymyoglobin in cardiomyocytes, it reacts at rates near the diffusion limit to form nitrate and methemoglobin (dioxygenation reaction).5,6 It will also react with the deoxyhemes of these proteins to form iron–nitrosyl complexes, which can release NO but inefficiently via the oxidative denitrosylation reaction.7 These 2 reactions, dioxygenation and iron nitrosylation, prevent NO from forming in the endothelium and diffusing to distant organ targets, such as the heart, intestine, kidney, brain, or liver.Article, see p 1601Despite the strict paracrine limitations imposed by this chemistry, several studies suggested that endocrine NO signaling is possible. The Kubes’ group showed that NO delivered by inhalation to cats could improve blood flow and limit inflammation in the cat intestine subjected to ischemia–reperfusion (I/R) injury8; Cannon et al6 later showed that this was possible in the human circulation. Many subsequent studies have shown that inhaled NO could rescue distal organs from I/R injury and infarction. In fact, upregulation of eNOS selectively in the heart could rescue the liver from I/R injury.9 However, free NO cannot account for these effects based on the short half-life of NO in blood, on the order …

Is Nitrite the Circulating Endocrine Effector of Remote Ischemic Preconditioning?