Nitric oxide (NO) is a vasoactive molecule that, by stimulated and functional vascular endothelial cells, is released to the lumen of the vessel and into the surrounding smooth muscle cells. Once in the lumen, NO is captured by red blood cells and scavenged inside through hemoglobin and derived as NO metabolites. The delivery ability of erythrocytes allowing the NO efflux also occurs. Manipulation of NO levels inside the erythrocyte through different external (acetylcholine, acetylcholinesterase inhibitors, fibrinogen and CD47 4N1K peptide) and internal (redox and protein phosphorylation levels) stimuli will be described. The values of NO efflux from the erythrocytes and its association with the data quantified in the hemorheology properties and in clinical parameters obtained from patients with vascular diseases will also be present. The in vivo animal experimental studies highlighting the ability of NO efflux (delivered) from the erythrocytes where is scavenged and its influence in inflammatory and hemorheological responses will be addressed. So, the aim of this chapter is to present the knowledge obtained about the NO signal transduction mechanism in erythrocytes and the association between erythrocyte availability in NO with clinical biomarkers obtained in inflammatory vascular diseases. A final question is raised—namely, could NO be considered a hemorheological parameter?
Part of the book: Novel Prospects in Oxidative and Nitrosative Stress