Computational model of NO and NO oxidative species transport in the microcirculation

Abstract

Sufficient availability of nitric oxide (NO) in the smooth muscles of blood vessels is important for its function as the proposed endothelium derived relaxing factor. NO may be preserved through the formation of NO2− anions or nitrosothiols which have a longer half‐life than NO in the circulation and thus may be transporting NO. A 2 D axisymmetric diffusion model was used to observe NO and NO oxidative species transport and to test the potential contribution of NO2− and nitrosothiols to smooth muscle NO levels according to data derived in previous research. With physiological concentrations of NO2− (10 μM – 20 μM) in the smooth muscle tissue, sufficient NO is generated to control blood vessel tone. NO2− reduction was more efficient in the lumen as compared to the tissue. Mitochondrial NO oxidase activity in the tissue regions was found to be an important factor for generating smooth muscle levels of NO2−. It was observed that the major nitrosating mechanism in the circulation is the •NO2 radical provided NO oxidation is accelerated in the hydrophobic regions of tissue layers and nitrosothiols may deliver minor amounts of NO through the Cu+ dependent enzyme activity. This study was supported by the NIH grant SC1HL095101