ABSTRACT

The main source of vascular NO in mammals is from eNOS contained within the endothelial cells. The loss or uncoupling of eNOS impairs cerebrovascular function in part by promoting vasoconstriction, platelet aggregation, smooth muscle cell proliferation, leukocyte adhesion and greater endothelial-immune cell interaction.15-17 Vascular NO production from the endothelium is regulated by eNOS enzyme activity and/or NOS gene expression (Figure 19.1).