[Inhibition of platelet activation by endothelium-derived relaxing factor EDRF/NO and NO releasing dilator substances].
Several circulating agonists and hydromechanic factors such as the viscous drag-induced shear forces of the bloodstream stimulate the release of EDRF/NO from endothelial cells. Abluminally released EDRF controls vascular tone, luminally released EDRF diffuses into the platelets, especially when they come into contact with the endothelial cell lining. Stimulating soluble guanylate cyclase in the platelets causes a rise in cGMP and a reduction in intracellular Ca(2+)-concentrations which suppresses platelet adhesion and aggregation, and potentiates the effects of PGI2-induced cAMP-increases. Nitrovasodilators which spontaneously release NO, such as molsidomine and sodium nitroprusside, can substitute for diminished EDRF-release from deficient endothelial cells and, likewise, suppress platelet aggregation in vitro and in vivo.
Bassenge
E
E
Institut für Angewandte Physiologie, Universität Freiburg.
D000818:Animals; D001161:Arteriosclerosis / Q000097:blood; D006801:Humans; D008981:Molsidomine / Q000031:analogs & derivatives* / Q000494:pharmacology; D009569:Nitric Oxide / Q000097:blood / Q000494:pharmacology* / Q000502:physiology; D010974:Platelet Aggregation / Q000187:drug effects* / Q000502:physiology; D013927:Thrombosis / Q000097:blood; D014665:Vasodilator Agents / Q000494:pharmacology*
D014665:Vasodilator Agents; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine
Hemmung der Plättchenaktivierung durch Endothelium-derived Relaxant Factor EDRF/NO und NO-freisetzende Dilator-Substanzen.