[Endothelial factors and thrombocyte function].
Platelet activity in circulating blood is controlled by platelet-vessel-wall interactions. This includes the generation of endothelium-derived factors, such as the arachidonic acid metabolite prostacyclin and endothelium-derived relaxing factor (EDRF), probably NO, generated from L-arginine. Both compounds inhibit platelet function and are arterial vasodilators. Endothelial dysfunction, e.g. during advanced atherosclerosis, is associated with reduced local formation of these compounds. This may result in platelet hyperreactivity and an increased risk of acute thrombembolic complications. Exogenous administration of synthetic PGI2-mimetics inhibits platelet function. This is a short-term action and the dosage is limited by systemic hypotension. NO-donators (molsidomine, organic nitrates) inhibit platelet-related vasospasm in stenosed coronary arteries in animal experiments. The significance of antiplatelet effects of organic nitrate vasodilators regarding their antianginal effectivity requires further study.
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Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf.
D000818:Animals; D001161:Arteriosclerosis / Q000097:blood* / Q000188:drug therapy; D001792:Blood Platelets / Q000187:drug effects / Q000502:physiology*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000503:physiopathology*; D011464:Epoprostenol / Q000502:physiology*; D006801:Humans; D008981:Molsidomine / Q000031:analogs & derivatives / Q000627:therapeutic use; D009569:Nitric Oxide / Q000097:blood / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects / Q000502:physiology; D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents / Q000627:therapeutic use
D010975:Platelet Aggregation Inhibitors; D014665:Vasodilator Agents; D009569:Nitric Oxide; C002385:linsidomine; D008981:Molsidomine; D011464:Epoprostenol
Endotheliale Faktoren und Thrombozytenfunktion.