Relationship between cyclic AMP and thromboxane formation in platelet-endothelial cell interactions.
Human platelet aggregation was triggered in the presence of various numbers of cultured endothelial cells. Thromboxane B2 formation and platelet cyclic AMP were also measured. Using a low concentration of thrombin (0.025U/ml) as aggregating agent, the inhibition of platelet aggregation correlated with that of thromboxane formation and was directly related to both the number of endothelial cells and platelet cyclic AMP. In contrast, using arachidonic acid (10(-5)M) instead of thrombin, platelet aggregation could be abolished although thromboxane formation was not affected. These results suggest that platelet aggregation induced by low concentrations of thrombin might be dependent on prostaglandin endoperoxides/thromboxane A2 production which could be inhibited by cyclic AMP. The normal synthesis of thromboxane B2 from exogenous arachidonate indicates that cyclic AMP is only active upon the liberation of endogenous arachidonate from platelet phospholipids.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D016718:Arachidonic Acid; D001095:Arachidonic Acids / Q000494:pharmacology; D001792:Blood Platelets / Q000378:metabolism*; D000242:Cyclic AMP / Q000097:blood*; D004727:Endothelium / Q000502:physiology; D011464:Epoprostenol / Q000097:blood; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects; D013917:Thrombin / Q000494:pharmacology; D013929:Thromboxane B2 / Q000097:blood*; D013931:Thromboxanes / Q000097:blood*
D001095:Arachidonic Acids; D013931:Thromboxanes; D016718:Arachidonic Acid; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D000242:Cyclic AMP; D013917:Thrombin