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The remodeling of blood vessels, characterized by thickening of the vessel wall attributable to neointima formation or changing of the vessel wall thickness and diameter, occurs after injury, dysfunction, or endothelial denudation, resembling the risk associated with endovascular surgery. Upon vascular injury, activated vascular smooth muscle cells (VSMCs) of local or systemic origin contribute to the remodeling processes which may eventually lead to occlusion of the blood vessel.1 Thus, understanding the molecular aspects of occlusive neointimal proliferation is desirable to promote better therapies for this disease process.See accompanying article on page 1244 There is substantial evidence that endothelial-derived nitric oxide (NO) is a key regulator of vascular remodeling.2,3 Endothelial nitric oxide synthase (eNOS)-derived NO diffuses into the surrounding cell layers of VSMCs to exert various cardiovascular homeostatic functions. eNOS can be stimulated to produce NO by hemodynamic forces, autacoids, hormones, and growth factors. Once NO diffuses into the VSMC layer, NO mediates vasorelaxation but also regulates the balance of VSMC proliferation versus apoptosis, the latter functions governing important aspects of vessel caliber and remodeling.4 Thus, one can envision …

Are the Mechanisms for NO-Dependent Vascular Remodeling Different From Vasorelaxation In Vivo?