Figure 2.

Cell surface targets for the antithrombotic action of S-nitrosothiols (RSNOs). Inhibition of the thrombotic process may be mediated without the need for intracellular nitric oxide (NO) entry, by inactivation of platelet surface adhesion molecules and/or of tissue factor exposed on the surface of the damaged vascular wall, on activated monocytes or circulating microparticles. These modifications occur indirectly via RSNO-induced inhibition of cell surface protein disulphide isomerase (csPDI), and also possibly via direct transnitrosation of the target molecule.