The role of von Willebrand factor (vWF) in mediating platelet adhesion has been established with the use of in vitro perfusion systems. vWF binds to the subendothelium, changes in conformation, and is then able to interact with glycoprotein Ib. vWF deposited in the subendothelium is responsible for up to 40% of normal adhesion. The action of vWF is seen at high shear rates. It also acts at low shear rates, but other factors can assume its role. Binding of vWF to the subendothelium is not through the established collagen binding sites but involves a new domain on the vWF molecule. Collagen VI has been implicated as the vessel wall component involved. Deposition of vWF in the subendothelium is determined by growth conditions and activation state of the endothelial cell. Subendothelial vWF in von Willebrand's disease may support platelet adhesion in situations in which plasma vWF of the same patient does not.