Abstract
Nitric oxide (NO) is accepted to be an important factor affecting the degree of vascular tone in various portions of the circulation. Until recently, research in this area has focused on endothelial cells as a NO source, and there is general agreement that: 1) the level of wall shear stress is the primary determinant of endothelial nitric oxide synthase (eNOS) expression; 2) exercise training induces changes of endothelial cell NO synthesizing activity; 3) phosphorylation patterns of eNOS are altered following exercise episodes. However, there is now a growing body of evidence for the existence of similar nitric oxide synthesizing mechanisms in human red blood cells (RBC). Erythrocyte NOS activity has been demonstrated to be induced by applied shear stress and mechanical deformation of RBC, and there are closely linked increases of intracellular nitric oxide levels and of release of NO into the suspending phase. In brief, the RBC is an enzymatic source of NO that is dependent on flow dynamics and from which NO is released in very close proximity to vessel walls. Although reports regarding the influence of exercise on RBC nitric oxide synthesizing mechanisms are not yet concordant, it seems logical to suggest that this source of NO may play a role in the regulation of local blood flow dynamics during exercise.