Results: 2

Figure 1

Figure 1. From: Vascular nitric oxide: formation and function.

Biological reactions of nitric oxide. The free radical nitric oxide (NO·) can react with many constituents within the vasculature that affect its bioavailability. NO· can undergo oxidative inactivation (reactions shown in dashed lines) to form nitrite ( ) and nitrate ( ). Other biologically relevant mechanisms include indirect interaction with hydrogen peroxide (H2O2) products (via Fenton chemistry) resulting in nitrous acid (HNO2) formation. Another key reactive oxygen species in the vasculature contributing to NO insufficiency is superoxide ( ) which reacts with NO to form peroxynitrite (OONO). S-nitrosothiols (RSNO) formation via OONO interaction with thiols, and nitrosyl-heme/S-nitroso-albumin formation represent ways in which NO can be protected from oxidative inactivation, thereby increasing overall bioavailability.

Richard C Jin, et al. J Blood Med. 2010;1:147-162.
Figure 2

Figure 2. From: Vascular nitric oxide: formation and function.

Factors and actions affecting NO and platelet function. Nitric oxide (NO) exerts inhibitory effects (dashed lines) on platelets through a variety of mechanisms. The predominant pathway involves generation of NO from l-arginine by endothelial nitric oxide synthase (eNOS) and cyclic guanosine monophosphate (cGMP) formation via guanylyl cyclase activation by NO. Nitric oxide inhibits platelet activation and aggregation by decreasing intracellular Ca2+ concentration, glycoprotein (GP) IIB/IIIa expression, and platelet association with fibrinogen. cGMP, formed from NO’s catalytic effect on guanylyl cyclase, also inhibits platelets by decreasing thromboxane A2 expression as well as expression of the platelet surface adhesion molecule, P-selectin. Endothelial NOS activity is regulated by several transcriptional, posttranslational, and physiological factors that either result in inactivation or upregulation, ultimately affecting NO bioavailability. Factors decreasing eNOS (dashed lines) activity include NO itself, via negative feedback, reduced substrate and/or cofactor bioavailability, hypoxia, and oxidized low density lipoprotein (LDL). By contrast, laminar shear stress, cell growth, and H2O2 have been shown to increase eNOS activity (solid lines), cGMP formation, and bioavailable NO.

Richard C Jin, et al. J Blood Med. 2010;1:147-162.

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