ATP- and ADP-induced rat platelet aggregation: significance of plasma in ATP-induced aggregation
Haskel, E.J.; Agarwal, K.C.; Parks, R.E.
Thrombosis and Haemostasis 42(5): 1580-1588
1980
ISSN/ISBN: 0340-6245 PMID: 7368159 Document Number: 160258
ATP caused platelet aggregation in rat platelet-rich plasma (PRP) but in contrast strongly inhibited ADP-induced human platelet aggregation. ADP-induced aggregation of rat platelets suspended in human plasma was strongly inhibited by ATP, whereas human platelets in rat plasma were aggregated by ADP. The ATP analog .beta.,.gamma.-methylene ATP which is not dephosphorylated did not induce aggregation in rat PRP. Adenosine, AMP, 2-chloroadenosine, .alpha.,.beta.-methylene ADP and .beta.,.gamma.-methylene ATP each inhibited ATP-induced aggregation of platelets in rat PRP to a similar extent as ADP-induced aggregation. A solution containing creatine kinase and creatine phosphate (which converts ADP to ATP) rapidly reversed ADP- and ATP-induced aggregation in rat PRP; preincubation with this solution completely inhibited rat platelet aggregation induced by ADP and ATP. [14C]-ATP conversion to [14C]-ADP was about 5-fold faster in rat plasma than in human plasma. Addition of creatine phosphate to rat PRP strongly inhibited ATP-induced aggregation, while creatine or creatine kinase slightly potentiated aggregation by ATP. Creatine phosphate, creatine or creatine kinase individually had minimal and varying effects on ADP-induced rat platelet aggregation. The observed phenomenon of ATP-induced aggregation in rat PRP is apparently caused by higher activity of creatine kinase in rat plasma than in human plasma, which converts the added ATP to ADP, a potent aggregator.