This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. A loss of endothelial dependent vasodilation (EDV), specifically the loss of endothelial-derived NO, constitutes the central feature of vascular endothelial dysfunction. Impaired EDV is present in major risk factors for CVD, such as age and hypercholesterolemia and a predictor for suture cardiovascular events. Therefore, there is currently a great need to determine the mechanisms associated with the pathogenesis of impaired EDV in these physiological/pathophysiological states. Recent experimental indicate that CYP-450, one of the sources of vascular oxidative stress, might play a role in the impaired EDV found in patients with coronary artery disease. However, it is unknown whether CYP 450 impairs EDV in patients with hypercholesterelomia and with healthy aging.
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