Kinetic differences between thrombin-induced and ADP-induced calcium influx and release from internal stores in fura-2-loaded human platelets.
The rapid (less than 1 sec) time course of [Ca2+]i rises was measured in fura-2-loaded, aspirin treated human platelets by stopped flow fluorimetry. With thrombin, which is known to cause substantial, rapid hydrolysis of phosphatidylinositol-4,5-bisphosphate, the mean delay before a detectible rise in [Ca2+]i in medium containing 1 mM Ca2+ o was 250 +/- 10 msec (S.E.M., n = 11). With ADP, which is reported not to stimulate phosphatidylinositol-4,5-bisphosphate hydrolysis, the delay under the same conditions was only 20 +/- 10 msec (S.E.M., n = 26). In the absence of external Ca2+, with 1 mM EGTA, the measured delays were 300 +/- 20 msec for thrombin and 210 +/- 10 msec for ADP. Times to peak were also faster for ADP than thrombin. These results suggest that thrombin and ADP promote Ca2+ influx in different ways. It is also possible that the process generating Ca2+ influx differs from that which triggers release from internal stores.
D000244:Adenosine Diphosphate / Q000494:pharmacology*; D001572:Benzofurans / Q000494:pharmacology*; D001792:Blood Platelets / Q000187:drug effects / Q000378:metabolism*; D002118:Calcium / Q000097:blood*; D016257:Fura-2; D006801:Humans; D007700:Kinetics; D013050:Spectrometry, Fluorescence; D013917:Thrombin / Q000494:pharmacology*; D013997:Time Factors
D001572:Benzofurans; D000244:Adenosine Diphosphate; D013917:Thrombin; D002118:Calcium; D016257:Fura-2