Proposed model for the role of PDI in regulating vascular NO activity. In the quiescent vasculature, when NO levels are high, PDI may be S-nitrosylated. Endothelial SNO-PDI could transfer NO to surface proteins, thereby inhibiting their activity, or transfer NO intracellularly. Intracellular NO could bind to guanylyl cyclase, stimulating the generation of cGMP and contributing the platelet quiescence.