Contribution of ADP to the amplification of primary platelet aggregation by platelet activating factor (PAF): modulatory role of aspirin

Lauri, D; Cerletti, Chiara; Gaetano, Giovanni de

doi:10.1007/bf01965522

Cited by 5 publications

(3 citation statements)

References 27 publications

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“…Apyrase reduced aggregation induced by PLC and PLC + ADP, but did not affect aggregation induced by PLC in combina tion with another stimulus. The combination of aspirin and apyrase did not inhibit aggregation by paired stimuli (PLC + U-46619 and PLC + PAF) but it was reported to inhibit PAF-induced aggregation (23).…”

Section: Discussionmentioning

confidence: 88%

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

Barzaghi

Cerletti

1988

Thromb Haemost

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SummaryWe studied the aggregating effect of different concentrations of phospholipase C (PLC) (extracted from Clostridium perfringens) on human platelet-rich plasma (PRP). PRP was preincubated with PLC for 3 min at 37° C and the platelet aggregation was followed for 10 min. The threshold aggregating concentration (TAG) of PLC was 3-4 U/ml.We also studied the potentiation of PLC with other stimuli on platelet aggregation. Potentiating stimuli, such as arachidonic acid (AA), ADP. Platelet Activating Factor (PAF) and U-46619 (a stable analogue of cyclic endoperoxides) were all used at subthreshold concentrations. We also studied the possible inhibitory effect of aspirin, apyrase, TMQ, a prostaglandin endoper- oxide/thromboxane receptor antagonist and BN-52021, a PAF receptor antagonist. Only aspirin and apyrase were able to reduce aggregation induced by PLC alone and PLC + AA and PLC + ADP respectively. TMQ and BN-52021 were inactive. In ex vivo experiments oral aspirin (500 mg) partially inhibited platelet aggregation induced by PLC alone, PLC + AA and PLC + ADP 2 and 24 h after administration. Aspirin 20 mg for 7 days also reduced aggregation induced by PLC + AA.

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Section: Discussionmentioning

confidence: 88%

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

Barzaghi

Cerletti

1988

Thromb Haemost

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“…Thus the mechanism of release of alpha granules, as studied here, appears similar to that of dense granules. Indeed, PAF also induces secretion from dense granules in citrated PRP almost completely through the TX pathway [6,9,10,12,13,27]. Working on WP in the presence of Ca 2+, Vargaftig et al [28] found only partial release from dense granules after stimulation with PAF+ EPI.…”

Section: Discussionmentioning

confidence: 97%

“…Release of dense and alpha granules is triggered by the aggregating agents through different mechanisms. The strong agents, like thrombin and calcium ionophores, induce release even after blockade of the TX pathway, while ADP, epinephrine or low doses of collagen do not induce release when this pathway is not viable [5,13]. At variance with a recent paper [30] our data fully support the view [6] that PAF, although active at very low concentrations, should be considered a weak releasing agent, since the release reaction can only be induced when the thromboxane-endoperoxide receptor is stimulated, q-his is apparent in citrated PRP, where BTG release was inhibited by either cyclooxygenase or receptor blockade, and is also supported by the data on WP in the presence of calcium, where PAF did not induce TXB2 synthesis and BTG release was low.…”

Section: Discussionmentioning

confidence: 99%

At low extracellular calcium concentration platelet activating factor induces beta-thromboglobulin release from human platelets through thromboxane-endoperoxides formation

et al. 1987

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The aim of this study was to investigate the mechanism involved in beta-thromboglobulin (BTG) release induced by platelet activating factor (PAF) in human platelet-rich plasma (PRP) and washed platelets (WP) during aggregation. PAF was used in PRP at increasing concentrations starting at its threshold concentration for irreversible aggregation (TAC: 90-150 nM). In citrated PRP, PAF induced release of BTG (80-95% of total content) and thromboxane B2 (TXB2) formation (30-40 pmol/ml). At low PAF concentrations aggregation and BTG release were blocked by apyrase (a scavenger of ADP), by ASA (an inhibitor of cyclooxygenase) and by BM 13177 (a thromboxane receptor antagonist). Higher concentrations of PAF overcame the effect of apyrase, but only induced reversible aggregation and minor release in the presence of ASA or BM 13177. In heparinized PRP, PAF induced full irreversible aggregation, but only very low BTG release (about 25% of total content) and thromboxane synthesis (2-3 pmol/ml). WP resuspended in the presence of 2 mmol/l Ca2+ seldom responded to PAF alone, as previously shown by others, but full aggregation could be induced by concomitant addition of subthreshold concentrations of PAF (25-50 nM) and epinephrine (1 microM). In these conditions average BTG release from WP was less than 20% of the amount releasable by thrombin. In contrast, when WP were resuspended in the absence of Ca2+, stimulation by PAF + EPI induced sustained BTG release (40-50% of total content) and TXB2 synthesis (15-20 pmol/ml). We conclude that at low Ca2+ concentration PAF induces BTG release mainly through thromboxane-endoperoxides formation. In contrast, when [Ca2+] is normal, PAF does not or weakly induces thromboxane formation and BTG release.

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The effect of AD6 (8-monochloro-3-β-diethylamino-ethyl-4-methyl-7-ethoxycarbonylmethoxycoumarin) on washed human platelet aggregation induced by platelet activating factor (PAF) and epinephrine

Zanetti

Zatta

Prosdocimi

et al. 1986

European Journal of Pharmacology

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Contribution of ADP to the amplification of primary platelet aggregation by platelet activating factor (PAF): modulatory role of aspirin

Cited by 5 publications

References 27 publications

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

Phospholipase C from Clostridium Perfringens Induces Human Platelet Aggregation in Plasma

At low extracellular calcium concentration platelet activating factor induces beta-thromboglobulin release from human platelets through thromboxane-endoperoxides formation

The effect of AD6 (8-monochloro-3-β-diethylamino-ethyl-4-methyl-7-ethoxycarbonylmethoxycoumarin) on washed human platelet aggregation induced by platelet activating factor (PAF) and epinephrine

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