Endothelial dysfunction is a marker of atherosclerosis and contributes to the atherogenic process and the development of atherothrombotic complications. Oxidative stress has been implicated in the development of endothelial dysfunction through alterations of the nitric oxide metabolism.
A number of evidence suggests a role for phagocytic-cell-mediated oxidative stress in diminished nitric oxide availability that is present in patients with atherosclerotic risk factors such as arterial hypertension. Thus, the combination of an excessive production of reactive oxygen species, namely superoxide anion, with an impaired antioxidant defense capacity leading to oxidative stress may facilitate the development and progression of atherosclerosis.
Findings from recent clinical studies suggest that this mechanism can be operative in patients with cerebrovascular disease. This view may increase our capabilities to understand the pathophysiology of cerebrovascular disease, as well as to stimulate the design of new therapeutic strategies aimed to prevent and control the atherosclerotic process in patients presenting this condition.
CITA DEL ARTÍCULO Cerebrovasc Dis. 2007;24 Suppl 1:24-9. Epub 2007 Nov 1