Abstract
THERE is considerable interest in the effects of prostaglandins on blood platelets, partly because the synthesis of prostaglandins by stimulated platelets is important in haemostasis, and partly because platelets can be used as models to investigate the actions of prostaglandins (PGs) at a cellular level1. The effects of different PGs on platelets are diverse: PGE1 is a potent inhibitor of platelet aggregation2 with a Ki value around 30 nM and PGD2 is an even more effective inhibitor of aggregation of human platelets, but not those of some other species3,4. PGE2 inhibits platelet aggregation at high concentrations (> 1 × 10−6 M), and there is some controversy as to whether lower concentrations enhance aggregation5. When human platelets are stimulated by collagen they synthesise PGE2 from arachidonic acid6 and the cyclic endoperoxide intermediates in the biosynthesis of PGE2 exert a direct aggregating effect7,8. Synthetic derivatives of PGE2 can also induce the aggregation of human platelets9, but PGE2 itself has never been found to induce aggregation directly.
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University Department of Pathology, Tennis Court Road, Cambridge, CB2 1QP, UK.
- D. E. MACINTYRE
- & J. L. GORDON
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