[Endothelial dysfunction and coronary heart disease. Interaction of endothelium and thrombocytes].
Aggregating thrombocytes release various mediators acting on endothelium and muscle cells of coronary arteries. In coronary arteries without endothelium, platelets induce potent vasoconstriction, whereas in segments with endothelium platelets induce relaxation. This endothelium-dependent relaxation induced by platelets is caused by the endothelial relaxation factor EDRF or nitric oxide (NO). NO inhibits not only smooth muscle cells of the vessels but also platelets themselves, an effect which is potentiated by prostacyclin. The physiologic importance of platelets-mediated contraction after removal of the vascular endothelium concerns the vascular phase of hemostasis. With the appearance of functional endothelial disorders, particularly in patients with cardiovascular risk factors, disturbances of coronary circulation can arise and finally cause ischemia. The finding that regenerated endothelial cells show functional defects especially towards the action of platelets (mainly the serotonin released from platelets) is important. In this functional disorder a dysfunction of Gi-protein of the endothelial 5HT1-serotonergic receptor plays a decisive role. Similar functional endothelial disorders can be shown after ischemia and reperfusion as well as in arteriosclerosis.
Vanhoutte
P M
PM
Center for Experimental Therapeutics, Baylor College of Medicine, Houston, TX 77030.
D000818:Animals; D001792:Blood Platelets / Q000502:physiology*; D003326:Coronary Circulation / Q000502:physiology; D003327:Coronary Disease / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D011464:Epoprostenol / Q000502:physiology; D006801:Humans; D009569:Nitric Oxide / Q000502:physiology; D010974:Platelet Aggregation / Q000502:physiology
D009569:Nitric Oxide; D011464:Epoprostenol
Endotheliale Dysfunktion und koronare Herzkrankheit. Interaktion von Endothel und Thrombozyten.