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Capsaicin, the 'hot' principle found in chilli, and other vanilloids exert their effects on neuronal cells through activation of transient receptor potential vanilloid 1 (TRPV1). TRPV1 is widely distributed in neuronal and non-neuronal cells. It has been proposed that consumption of vanilloid-like agents, including capsaicinoids, inhibits platelet aggregation and may protect against the development of cardiovascular disease. The aim of this study was to investigate the effects of a range of vanilloid-like agents on in vitro platelet aggregation. Venous blood was collected from healthy subjects who avoided antiplatelet medications and dietary chilli for at least 10 and 2 days, respectively. Collagen (4 and 8 ˜í¬¿g/mL), ADP (10 and 5 ˜í¬¿M) and arachidonic acid (AA) (300 and 400 mg/mL) -induced platelet aggregation was determined using platelet rich plasma (PRP; \\(250x10^9L\\)) in the absence and presence of the capsaicinoids [capsaicin and dihydrocapsaicin (DHC)] and the endocannabinoid/endovanilloid agents [Noleoyldopamine (OLDA) and N-arachidonoyl-dopamine e (NADA)]. %Maximum aggregation (%Max), % area under curve (%AUC) and slope of platelet aggregation were determined. Platelet lactate dehydrogenase (LDH), which is released rapidly after cell membrane damage, was investigated to determine the direct toxic effects of these agents on platelets. Platelet factor 4 (PF4) and ˜í‚â§-thromboglobulin (˜í‚â§-TG) release were examined to determine the effects of vanilloids on alpha granule release. Finally, the effects of TRPV1 antagonist (SB-452533) on capsaicin- and OLDA-mediated inhibition of ADP-induced platelet aggregation were investigated. ADP-induced (5 ˜í¬¿M) platelet aggregation was inhibited in a concentration-dependent manner by capsaicin (%Max, mean ¬¨¬±SEM; 0 vs 100 ˜í¬¿M, 83.8¬¨¬±0.9% vs 45.2¬¨¬±2.4%, n=6, p>0.001); OLDA (0 vs 100 ˜í¬¿M, 71.6¬¨¬±8.2% vs 9.4¬¨¬±1.4%, n=4, p |
