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Specificity Between the Anti-Aggregatory Actions of Prostacyclin, Prostaglandin E1 And D2 on Platelets

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Mechanisms of Stimulus—Response Coupling in Platelets

Part of the book series: Advances in Experimental Medicine and Biology ((AEMB,volume 192))

Abstract

Of the naturally-occurring cyclo-oxygenase metabolites known as the prostaglandins, three such products, prostaglandin E1, prostaglandin D2 and prostacyclin have been demonstrated to exert potent anti-aggregating actions on platelets. Early studies indicated that prostaglandin E1 (PGE1) which is derived from the precursor fatty acid, dihomo-gamma-linoleic acid, could inhibit platelet aggregation in vitro in platelet-rich plasma (PRP) from several species (1,2,3). However, since only trace levels of PGE1 can be detected under normal dietary conditions in vivo (A), the physiological significance of the actions of this prostanoid remain obscure. Later studies with PGD2 (Fig 1) derived from the essential fatty acid arachidonic acid, likewise indicated this prostanoid to be a potent inhibitor of platelet aggregation in human platelet-rich plasma in vitro (5,6). In contrast to PGE1, the activity of PGD2 could not be readily demonstrated in the plasma of the rat or rabbit (7). Thus PGD2 is a potent inhibitor of platelet aggregation in human, sheep and horse platelet-rich plasma but only a weak inhibitor in dog, rabbit, guinea-pig and rat plasma (Table 1). PGD2 can be generated by human platelets and has been detected in human plasma (8,9,10), while the non-enzymatic conversion of the endoperoxide PGH2 to PGD2 is greatly enhanced by the presence of plasma protein from certain species including man (11,12).

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© 1985 Plenum Press, New York

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Whittle, B.J.R., Hamid, S., Lidbury, P., Rosam, A.C. (1985). Specificity Between the Anti-Aggregatory Actions of Prostacyclin, Prostaglandin E1 And D2 on Platelets. In: Westwick, J., Scully, M.F., MacIntyre, D.E., Kakkar, V.V. (eds) Mechanisms of Stimulus—Response Coupling in Platelets. Advances in Experimental Medicine and Biology, vol 192. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-9442-0_9

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  • DOI: https://doi.org/10.1007/978-1-4615-9442-0_9

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