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. 1992 Aug;106(4):917–923. doi: 10.1111/j.1476-5381.1992.tb14435.x

Potentiation of ADP-induced aggregation in human platelet-rich plasma by 5-hydroxytryptamine and adrenaline.

D M Vanags 1, S E Rodgers 1, E M Duncan 1, J V Lloyd 1, F Bochner 1
PMCID: PMC1907675  PMID: 1393289

Abstract

1. We have used dose-response curves to quantitate the potentiation of adenosine 5'-diphosphate (ADP)-induced aggregation and thromboxane (TXA2) generation by 5-hydroxytryptamine (5-HT) and adrenaline in human citrated platelet-rich plasma. We have also quantitated the inhibition of these responses by aspirin, ketanserin and yohimbine, singly and in pairs. 2. Ketanserin (5 microM) inhibited TXA2 production and the second wave of platelet aggregation induced by a range of concentrations of ADP alone. This indicates that endogenous 5-HT, released from the platelet dense granules, contributes significantly to responses induced by ADP. 3. When 5-HT (10 microM) was added before ADP, a lower concentration of ADP was required to cause 50% aggregation and TXA2 generation. The ratio of ADP concentrations (CR) to cause 50% aggregation in the presence and absence of 5-HT was 2.1 when only added 5-HT was considered, and 5.0 when endogenous 5-HT was also taken into account. 4. Potentiation of ADP-induced aggregation by 5-HT also occurred in the presence of aspirin, resulting in a CR of 2.3. As expected, ketanserin inhibited potentiation by 5-HT in the presence and absence of aspirin. Although aspirin caused substantial inhibition of aggregation induced by ADP and 5-HT (CR 3.4), further inhibition occurred when ketanserin was also present (CR 6.5). 5. A subthreshold concentration of adrenaline (0.25 microM) caused substantial potentiation of ADP-induced aggregation in the absence (CR 4.0) and presence (CR 2.0) of aspirin. As expected, yohimbine (9 microM) inhibited this potentiation.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selected References

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