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A biochemical pathway analysis of endothelial NOS uncoupling

In diseased conditions such as hyperglycaemia, there is increased production of superoxide within the endothelial cells of the vasculature causing uncoupling of the enzyme eNOS present in endothelial cells. The uncoupling of eNOS results in increased eNOS based superoxide production and reduced production of the vasodilator NO leading to endothelial dysfunction. The uncoupling of eNOS occurs due to the diminishing availability of its co‐factor BH4, which under oxidative stress gets oxidized to its analogues BH3 and BH2. A kinetic model for eNOS based NO and superoxide production has been developed for this study. The model also incorporates the reaction kinetics for the scavenging of superoxide by SOD and the recycling of BH4 by ascorbate to ascertain their potential therapeutic effects. The simulations demonstrate that with increasing ascorbate concentrations there is an increase in NO production rate, decrease in superoxide production rate and an increase in the ratio of BH4 to BH2. Similar trends are also observed with SOD with the exception that the superoxide production rate remains unchanged with varying SOD concentrations. Supported by NIH R01 HL084337.