Contribution of a platelet component to endothelial prostacyclin production despite inhibition of platelet cyclooxygenase activity.
Platelets aggregated with low concentrations of thrombin enhanced prostacyclin release from umbilical vein endothelium, which had an active cyclooxygenase. This result cannot be explained solely by an effect of thrombin on the endothelium or by transfer of the endoperoxide PGH2 from platelets to the endothelium. The quantity of prostacyclin released is sufficient to alter platelet adherence to umbilical vein endothelium in the presence of thrombin.
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000818:Animals; D001011:Aorta / Q000378:metabolism; D001792:Blood Platelets / Q000201:enzymology*; D002417:Cattle; D004727:Endothelium / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation / Q000187:drug effects*; D011450:Prostaglandin Endoperoxides, Synthetic / Q000378:metabolism; D044262:Prostaglandin H2; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism*; D011453:Prostaglandins / Q000378:metabolism*; D011463:Prostaglandins H / Q000378:metabolism; D013917:Thrombin / Q000494:pharmacology*; D014471:Umbilical Veins / Q000378:metabolism
D011450:Prostaglandin Endoperoxides, Synthetic; D011453:Prostaglandins; D011463:Prostaglandins H; D044262:Prostaglandin H2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases; D013917:Thrombin