抄録
The endothelial dysfunction occurs in early stage of atherosclerosis. The assessment of flow-mediated dilation (FMD) is known as a noninvasive method to evaluate the endothelial function. FMD is induced by the following mechanisms: 1) the endothelial nitric oxide (NO) is released in response to the increase of flow stimuli and 2) NO acts on the vascular smooth muscle. The increasing oxidative stress such as smoking decreases FMD because the oxidative stress inhibits the endothelial NO synthase (eNOS) activation. Thus, FMD provides a diagnostic measure of the evaluation of the antismoking effect. According to clinical studies, the inhibition of eNOS activation by oxidative stress affects the magnitude of FMD. These studies suggest that transient features of FMD provides the information of endothelial dysfunction. However, the transient features have been few investigated due to the physiological complex signaling pathways. In this study, we developed a mathematical model which induces the NO production and the eNOS mechanisms. We performed numerical analysis of the properties of NO production under eNOS inhibition.
