Triphosphoinositide breakdown and dense body release as the earliest events in thrombin-induced activation of human platelets.
The activation by thrombin of human platelets prelabelled with 32P induced a 30-40% decrease in 32P-triphosphoinositides (TPI) in the first 10 sec; the decrease in the other 32P-labelled phosphoinositides occurred by 20-30 sec. At 10 sec., the intensity of these effects was maximum with 0.2-0.4 U/ml thrombin. Under these conditions, 53, 20 and 15% of the dense granule, alpha-granule and lysosome constituents, respectively were released and thromboxane B2 synthesis reached only 10% of its maximum. Together with experiments carried out with chlorpromazine - or PGE1 - treated platelets, our results suggest the existence of a close relationship between TPI-breakdown and dense body release which appear to be the earliest events resulting from the activation of human platelets by thrombin.
D001792:Blood Platelets / Q000187:drug effects* / Q000648:ultrastructure; D002746:Chlorpromazine / Q000494:pharmacology; D006801:Humans; D009940:Organoids / Q000378:metabolism*; D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols / Q000097:blood*; D013917:Thrombin / Q000494:pharmacology*; D013997:Time Factors
D018129:Phosphatidylinositol Phosphates; D010716:Phosphatidylinositols; C018803:triphosphoinositide; D013917:Thrombin; D002746:Chlorpromazine