Figure 8

Schematic figure of the role of cGK and sildenafil treatment in the vessel and platelets. After vascular injury such as balloon angioplasty or stent implantation, endothelial cells (ECs) are denuded, resulting in the downregulation of nitric oxide. Subsequently, the level of cGK in VSMCs and platelets decreases. VSMCs are converted to a synthetic form from a contractile form by the decreased cGK activity. Furthermore, the decreased cGK in platelets facilitates platelet aggregation. In addition, activated platelets produce PDGF which can stimulate VSMC proliferation. In contrast, sildenafil treatment can prevent the decrease of cGK activity in VSMCs and platelets, leading to the inhibition of both neointimal growth and platelet aggregation.