The Effects of Vanilloid-Like Agents on Platelet Aggregation

摘要: 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 non-neuronal cells. It has been proposed that consumption vanilloid-like agents, including capsaicinoids, inhibits platelet aggregation may protect against development of cardiovascular disease. The aim this study was to investigate effects a range of agents on vitro aggregation. Venous blood collected from healthy subjects who avoided antiplatelet medications dietary chilli for at least 10 2 days, respectively. Collagen (4 and 8 μg/mL), ADP (10 5 μM) arachidonic acid (AA) (300 400 mg/mL) -induced determined using rich plasma (PRP; 250x10 9/L) absence presence capsaicinoids [capsaicin and dihydrocapsaicin (DHC)] endocannabinoid/endovanilloid [Noleoyldopamine (OLDA) N-arachidonoyl-dopamine e (NADA)]. %Maximum aggregation (%Max), % area under curve (%AUC) slope aggregation were determined. Platelet lactate dehydrogenase (LDH), which released rapidly after cell membrane damage, investigated determine direct toxic of these platelets. factor 4 (PF4) β-thromboglobulin (β-TG) release were examined alpha granule release. Finally, antagonist (SB-452533) capsaicin- and OLDA-mediated inhibition ADP-induced investigated. (5 inhibited concentration-dependent manner by capsaicin (%Max, mean +/-SEM; 0 vs 100 μM, 83.8=/-0.9% 45.2+/-2.4%, n=6, p0.001); OLDA (0 71.68.2% 9.41.4%, n=4, and NADA 71.5+/-5.9% 38.2+/-1.4%, p0.008). Similar results were observed μM ADP. NADA, but not DHC, inhibited induced 4μg/mL collagen: (Max%, 100 μM, 89.3+/-1.4% 45.5+/-12.5%, p<0.001); NADA 87.7+/-0.8% vs 28.5+/-8.2%, p<0.001). AA-induced mg/mL) a concentration-dependent manner 89.6=/-0.9% vs 11+/-0.8%, DHC 88.3+/-2.1% 18.7+/-6.9%, 84+/-1.8% 21.9+-4.7%, 400mg/mL AA. all agents was due as LDH release platelets unaffected by any vanilloids. SB-452533 did inhibit (SB-45253; Max 10μM, 55.9+/-2.1% 58.4+/-1.37%) (SB-45253; Max vs 10μM, 65.15+/-0.44% 65.55+/-1%) aggregation, suggesting that inhibition mediated. ADP-stimulated PF4 release impaired capsaicin, whereas NADA enhanced PF4 release. Furthermore, impaired the β-TG platelets. The present human shows DHC, aggregation. inhibitory are not TRPV1 mediated effect Vanilloids interfering with granule release, although further investigation possibility warranted.