Letter from the Editor

Abstract Prostacyclin, nitric oxide and tissue plasminogen activator constitute a prominent triad of endothelial mediators. Prostacyclin is responsible mainly for maintaining vascular thromboresistance against platelet clumps, inhibits proliferation of vascular smooth muscle and modulates cholesterol turnover, tissue plasminogen activator is a fibrinolytic agent and nitric oxide controls vascular tone and structure. Receptor agonists such as acetylcholine, kinins, endothelins or adenosine diphosphate evoke a coupled release of mediators from endothelial cells. Prostacyclin and nitric oxide synergize in their antiplatelet, fibrinolytic and cardioprotective, but not in their hypotensive actions. Prostacyclin, but not nitric oxide, prevents paradox thrombogenic effects of tissue plasminogen activator. Filogenetically, prostacyclin and tissue plasminogen activator are younger brothers of nitric oxide from which they take over and perfect regulatory properties in circulation. Further studies on interactions of endothelial mediators may lead to a better understanding of mechanisms of thrombosis, atherogenesis, diabetic angiopathies, endotoxic shock and arterial hypertension.