Abstract
Endothelium-derived nitric oxide (NO) plays a key role in vascular functions including smooth muscle tone regulation, platelet activation and cell signaling. Substantial evidence indicates that the oxidative stress or the formation of reactive oxygen (e.g. superoxide) and nitrogen species (e.g. peroxynitrite) contributes to impairment of endothelium-dependent vasodilation and results in tyrosine nitration. The biochemical interactions of these reactive species on the tyrosine nitration in microcirculation remains unclear. We formulated a detailed computational model of NO, superoxide and peroxynitrite transport in a tissue containing an arteriolar blood vessel to study the tyrosine nitration in several regions of microcirculation including endothelium, smooth muscle and parenchyma. The biochemical interactions of NO, superoxide and peroxynitrite in the microvascular tissue are quantified. The model predictions indicate that the NO interaction with superoxide and peroxynitrite and resulting tyrosine nitration formation depends on the location of oxidative stress. The results are significant because the tyrosine nitration is observed in many pathological conditions but cellular sources for superoxide varies in different disease states. Supported by American Heart Association National SDG #0530050N and Arkansas Biosciences Institute (ABI).
Published Version
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