Influence on thromboxane and malondialdehyde synthesis in human thrombocytes by various inhibitors of platelet function.
The effects of various inhibitors of platelet function have been compared with respect to the minimal effective concentration required to inhibit platelet aggregation and the thromboxane (TXA2) and malondialdehyde (MDA) synthesis in washed platelets. The potencies of the agents in the different platelet function tests showed no consistent correlation. The most striking difference was found between the prostaglandins and the adenine nucleotides. The prostaglandins PGE1 and PGI2 inhibited all platelet reactions (10(-7) - 10(-8) g/ml) which may be explained by their stimulation of adenylcyclase. In contrast, the adenine nucleotides adenosine and AMP which are supposed to raise cAMP platelets via the same mechanism and strongly inhibited primary and secondary platelet aggregation (3 x 10(-6) - 3 x 10(-7) g/ml) had no effect on TXA2 and MDA synthesis. The results suggest that the pharmacological inhibition of platelet function may not act via a uniform mechanism controlled by the arachidonate pathway.
D000227:Adenine Nucleotides / Q000494:pharmacology; D000818:Animals; D001011:Aorta; D001095:Arachidonic Acids / Q000097:blood; D001681:Biological Assay; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D003094:Collagen / Q000097:blood; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008314:Malonates / Q000097:blood*; D008315:Malondialdehyde / Q000097:blood*; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology; D011817:Rabbits; D013917:Thrombin / Q000494:pharmacology*; D013928:Thromboxane A2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*
D000227:Adenine Nucleotides; D001095:Arachidonic Acids; D008314:Malonates; D011453:Prostaglandins; D013931:Thromboxanes; D008315:Malondialdehyde; D013928:Thromboxane A2; D003094:Collagen; D013917:Thrombin; D007213:Indomethacin