The role of platelet-activating factor (PAF) in aggregation of human platelets

• Published in: Blood & Vessel Vol. 19; no. 2; pp. 179 - 182
• Main Authors: SATOH, Kei, KAWAMURA, Yoko, IMAIZUMI, Tada-atsu, YOSHIDA, Hidemi, TAKAMATSU, Shigeru
• Format: Journal Article
• Language: English
• Published: The Japanese Society on Thrombosis and Hemostasis 1988
• Subjects: ADP; collagen; platelet aggregation; platelet-activating factor; thrombin
• ISSN: 0386-9717; 1884-2372
• DOI: 10.2491/jjsth1970.19.179

The role of platelet-activating factor (PAF) in human platelet function was studied by examining the possible involvement of PAF in agonist-induced aggregation and the mechanism by which PAF exerts its aggregating activity. Platelet aggregation induced by PAF was inhibited by aspirin or 5′-p-fluorosulfonylbenzoyl adenosine (FSBA), an inactive ADP analogue. The combined use of these two agents (each at 5μM) completely abolished PAF-induced second-wave aggregation in all platelet samples tested. We next examined the effect of a PAF-antagonist, CV-3988, on platelet aggregation. Pretreatment of platelets with 1-50μM CV-3988 slightly, but in a dose-dependent manner, inhibited the aggregation in response to 0.2U/ml thrombin. This antagonist had no effect on ADP- and collagen-induced aggregation. PAF production by washed human platelets was studied by measuring [3H] acetate incorporation into [3H] PAF. [3H] PAF production in response to 10μM ADP, 5μg/ml collagen or 2U/ml thrombin were 263±136.7, 1, 021±763.6 and 1, 112±628.9dpm/108 platelets, respectively (Mean±SD, n=3). The production by unstimulated controls was 412±207.6dpm/108 platelets. These results suggest that most part of the activity of PAF towards platelets may depend on thromboxane A2 and ADP. Platelets synthesize PAF in response to collagen and thrombin, and thrombin-induced platelet aggregation may be partly dependent on the generation of PAF.