Effect of thromboxane A 2 synthetase inhibition, singly and combined with thromboxane A 2 /prostaglandin endoperoxide receptor antagonism, on inositol phospholipid turnover and on 5-HT release by washed human platelets
European Journal of Pharmacology: Molecular Pharmacology, ISSN: 0922-4106, Vol: 188, Issue: 2, Page: 161-169
1990
- 6Citations
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Metrics Details
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Article Description
Differential effects on human platelet function of thromboxane A 2 (TXA 2 ) synthetase inhibition singly and of TXA 2 synthetase inhibition combined with TXA 2 /prostaglandin endoperoxide receptor antagonism were revealed. using ridogrel as a probe. Ridogrel combines selective TXA 2 synthetase inhibition with TXA 2 /prostaglandin receptor antagonism in one molecule; in washed human platelets, the compound reduces the production of TXB 2 (IC 50 =1.3 × 10 −8 M) and increases that of PGF 2α, PGE 2, PGD 2 from [ 14 C]arachidonic acid. Additionally, at higher concentrations (K i = 0.52 × 10 −6 M), it selectively antagonizes the breakdown of inositol phospholipids, subsequent to stimulation of TXA 2 /prostaglandin endoperoxide receptors with U 46619. The latter happens in a competitive way with fast receptor association-dissociation characteristics. At low concentrations (1 × 10 −9 − × 10 −7 M) producing single TXA 2 synthetase inhibition, ridogrel reduces the collagen-induced formation of TXB 2 by washed platelets, but enhances [ 32 P]phosphatidic acid (PA) accumulation and [ 3 H]5-hydroxytryptamine (5-HT) release. At higher concentrations (1 × 10 −6 −1 × 10 −5 M) which additionally block U 46619-induced [ 32 P]PA accumulation, ridogrel inhibits the [ 32 P]PA accumulation and release of [ 3 H]5-HT by human platelets stimulated with collagen. These observations, corroborated by results obtained with OKY 1581, sulotroban, indomethacin and human serum albumin, suggest a causal role for prostaglandin endoperoxides in the stimulation by TXA 2 synthetase inhibition of platelet reactions to collagen. They reinforce the concept that TXA 2 synthetase inhibition-induced reorientation of cyclic endoperoxide metabolism, away from TXA 2 into inhibitory prostanoids, requires additional TXA 2 /prostaglandin endoperoxide receptor antagonism to achieve optimal anti-platelet effects.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/092241069090051X; http://dx.doi.org/10.1016/0922-4106(90)90051-x; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0025706351&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/2318257; http://linkinghub.elsevier.com/retrieve/pii/092241069090051X; http://api.elsevier.com/content/article/PII:092241069090051X?httpAccept=text/xml; http://api.elsevier.com/content/article/PII:092241069090051X?httpAccept=text/plain; https://linkinghub.elsevier.com/retrieve/pii/092241069090051X; http://dx.doi.org/10.1016/0922-4106%2890%2990051-x; https://dx.doi.org/10.1016/0922-4106%2890%2990051-x
Elsevier BV
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