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Inhibition of platelet aggregation by vanilloid‐like agents is not mediated by transient receptor potential vanilloid‐1 channels or cannabinoid receptors
Author(s) -
Almaghrabi Safa,
Geraghty Dominic,
Ahuja Kiran,
Adams Murray
Publication year - 2016
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.12569
Subject(s) - trpv1 , chemistry , cannabinoid receptor , capsaicin , receptor , am251 , pharmacology , agonist , cannabinoid receptor type 2 , cannabinoid , transient receptor potential channel , biochemistry , biology
Summary Vanilloid‐like agents, including capsaicin, N‐arachidonoyl‐dopamine and N‐oleoyldopamine inhibit platelet aggregation, however little is known about the precise mechanism(s) of action. The authors have previously shown that blocking of the capsaicin receptor, transient receptor potential vanilloid‐1 ( TRPV 1), does not interfere with capsaicin action during adenosine diphosphate ( ADP )‐induced aggregation. This research is extended to investigate the effect of these vanilloid‐like‐agents on platelet count, and to test whether the effect of these agents is mediated through TRPV 1 and/or cannabinoid ( CB 1 and CB 2) receptors in the presence of other agonists, including collagen and arachidonic acid. Incubation of platelets with each of the individual vanilloids, or with receptor antagonists of TRPV 1 ( SB 452533), CB 1 ( AM 251) and CB 2 ( AM 630), for up to 2 h did not significantly affect the platelet count. Similarly, the effect of individual vanilloids on the inhibition of platelet aggregation was not significantly different in the presence of receptor agonists compared to control, irrespective of the agonist used, suggesting that the inhibitory effect of vanilloids on platelet aggregation is independent of TRPV 1, CB 1 and CB 2 receptors. Further research on the antiplatelet activity of vanilloids should focus on mechanisms other than those associated with vanilloid receptors.