Interaction of thrombin and platelets with the vascular endothelium.
Thrombin is a potent stimulus for prostacyclin (PGI2) release from the vascular endothelium. Treatment of the endothelium with high concentrations of aspirin to block PGI2 formation was associated with increased platelet adherence in a system employing thrombin and 51Cr-labeled platelets. Addition of exogenous PGI2 to the aspirin-treated endothelium restored platelet adherence to the low baseline values. After an initial exposure of the endothelium to thrombin, the cultured endothelium was unable to respond to a second thrombin stimulus with release of PGI2. During this refractory period, the absence of PGI2 was associated with increased platelet adherence. Thus thrombin, an active coagulant and thrombogenic substance, has the capability to release PGI2, the most potent inhibitor of platelet aggregation known to exist in vivo.
D001241:Aspirin / Q000494:pharmacology; D001792:Blood Platelets / Q000502:physiology*; D001808:Blood Vessels / Q000502:physiology*; D004727:Endothelium / Q000187:drug effects / Q000502:physiology; D011464:Epoprostenol / Q000378:metabolism; D006487:Hemostasis; D006801:Humans; D010973:Platelet Adhesiveness / Q000187:drug effects; D010974:Platelet Aggregation / Q000187:drug effects; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D013917:Thrombin / Q000502:physiology*
D011448:Prostaglandin Antagonists; D011464:Epoprostenol; D013917:Thrombin; D001241:Aspirin