Summary
Platelet aggregation, secretion of 5-hydroxy tryptamine and production of thromboxane
B2 were monitored simultaneously in human platelet suspensions in the absence and presence
of cyclooxygenase or thromboxane synthetase inhibitors. Aggregation, secretion and
thromboxane B2 formation in response to either sodium arachidonate or epinephrine were blocked by
aspirin or by 1-N-butyl imidazole suggesting that thromboxane biosynthesis was an
essential requirement for platelet activation by these agents. In contrast, thrombin
and collagen could apparently induce aggregation and secretion via two pathways: at
low doses involving thromboxane production, but at higher doses by a direct mechanism
independent of thromboxane biosynthesis. In the case of ADP, inhibition of thromboxane
production blocked secretion but had little effect on aggregation, indicating that
secretion was probably dependent on thromboxane biosynthesis which probably occurred
as a result of aggregation. Thus it appears that although the processes of thromboxane
production, release of dense granule constituents and aggregation may often be intimately
linked, each process can occur independently of the other, depending upon the stimulus
used.
Keywords
Platelet aggregation - 5 HT secretion - Thromboxane B
2
