Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Matthews, J.S. et al.

Potentiation of aggregation and inhibition of adenylate cyclase in human platelets by prostaglandin E analogues.

1. The 16-phenoxy prostaglandin E analogue sulprostone consistently potentiates primary aggregation waves induced by adenosine 5'-diphosphate (ADP), PAF and 11,9-epoxymethano PGH2 (U-46619) in platelet-rich plasma from human donors. The effect is not blocked by the TP-receptor antagonists, EP 092 and GR 32191. The high potency of sulprostone (threshold concentration = 4-10 nM) and the weak block of sulprostone potentiation by the EP1-receptor antagonist, AH 6809 (pA2 = 4.3) suggest the involvement of EP3-receptors as opposed to EP1- or EP2-subtypes. 2. Eight prostaglandin E (PGE) analogues were compared against sulprostone for their effects on PAF-induced aggregation in human platelet-rich plasma ( PRP) in the presence of GR 32191 and the DP-receptor antagonist, BW A868C. PGE2 and 11-deoxy PGE2-1-alcohol showed evidence of both potentiating and inhibitory actions and butaprost showed only inhibitory activity at high concentrations. The remaining analogues always elicited potentiation, with the following potency ranking: sulprostone = 16,16-dimethyl PGE2 > MB 28767 > misoprostol > GR 63779X = 17-phenyl-omega-trinor PGE2. The results again indicate that EP3- rather than EP1- or EP2-receptors are involved. However, relative potentiating potency could be affected by differences in plasma protein binding and the very high sensitivity of the human platelet to prostacyclin (IP)-receptor-mediated inhibition (IC50 for the specific IP-receptor agonist cicaprost = 0.8 nM).(ABSTRACT TRUNCATED AT 250 WORDS)[1]

References

Potentiation of aggregation and inhibition of adenylate cyclase in human platelets by prostaglandin E analogues. Matthews, J.S., Jones, R.L. Br. J. Pharmacol. (1993) [Pubmed]

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