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Activation of rabbit blood platelets by anandamide through its cleavage into arachidonic acid
Author(s) -
Braud Sandrine,
Bon Cassian,
Touqui Lhousseine,
Mounier Carine
Publication year - 2000
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(00)01359-4
Subject(s) - anandamide , chemistry , cannabinoid , arachidonic acid , agonist , pmsf , cannabinoid receptor , platelet , platelet activation , pharmacology , receptor , biochemistry , endocrinology , medicine , biology , enzyme
Anandamide (ANA), a cannabinoid receptor ligand, stimulated platelet aggregation at concentrations similar to those of arachidonic acid (AA). The aggregating effect of ANA was inhibited by aspirin but not by SR‐141716, a cannabinoid receptor antagonist. In addition, HU‐210, a cannabinoid receptor agonist, failed to induce platelet activation. Radiolabelling experiments showed that exogenous ANA was cleaved by platelets into AA through a phenylmethylsulfonyl fluoride (PMSF)‐sensitive pathway. In agreement, PMSF was shown to abolish the aggregating effect of ANA. In conclusion, ANA is able to induce platelet activation via its cleavage by a PMSF‐sensitive amidase activity, leading to the release of AA which in turn activates platelets.