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AIM: To examine the signalling mechanisms involved in the synergistic interaction of 5-hydroxytryptamine (5-HT) and arachidonic acid (AA) in human platelet aggregation. METHODS: Blood was obtained from healthy human subjects, mixed with 3.8% sodium citrate (9:1), and centrifuged to prepare platelet rich plasma (PRP). Aggregation was monitored using a Dual-channel Lumi-aggregometer. The agonist-induced influx of Ca~(2+) was measured using Fura-2 AM. TXA_2 formation was studied using radiochemical method. RESULTS: Subthreshold concentration of 5-HT (2μmol/L) potentiated the effect of low dose of AA (0.2 mmol/L) in human platelets. This synergistic effect was blocked by 5-HT_2 receptor antagonist (methysergide IC_(50)=5.2 nmol/L; cyproheptadine IC_(50)=0.6 nmol/L), and thromboxane A_2 receptor antagonist (SQ 29 548; IC_(50)=30 nmol/L), showing that the effect is receptor-mediated. To examine the down-stream signalling pathways, we found that such an interaction was inhibited by calcium channel blockers (d
AIM: To examine the signaling mechanisms involved in the synergistic interaction of 5-hydroxytryptamine (5-HT) and arachidonic acid (AA) in human platelet aggregation. METHODS: Blood was obtained from healthy human subjects, mixed with 3.8% sodium citrate : 1), and centrifuged to prepare platelet rich plasma (PRP). Aggregation was monitored using a Dual-channel Lumi-aggregometer. The agonist-induced influx of Ca ~ (2+) was measured using Fura- 2 AM. TXA_2 formation was RESULTS: Subthreshold concentration of 5-HT (2 μmol / L) potentiated the effect of low dose of AA (0.2 mmol / L) in human platelets. This synergistic effect was blocked by 5-HT_2 receptor antagonist (methysergide IC_ (50) = 5.2 nmol / L; cyproheptadine IC 50 = 0.6 nmol / L) and thromboxane A 2 receptor antagonist (SQ 29 548; IC 50 = 30 nmol / L) To examine the down-stream signaling pathways, we found that such an interaction was inhibited by calcium c hannel blockers (d