PAF-acether (platelet-activating factor) was hypothesized as the mediator of the ADP
and thromboxane-independent activation of platelets induced by thrombin (Thr) and
by the snake venom glycoprotein convulxin (Cx). Aspirinized rabbit platelets self-desensitized
to PAF-acether were less responsive to low amounts of Thr, as expected if PAF-acether
would be formed, but were hyper-reactive to Cx, in contradiction with its hypothesized
mediating role. Aggregation by higher concentrations of Thr overcame inhibition. Experiments
with ADP-depleted platelets showed that secretion is neither involved with desensitization
to PAF-acether nor with hyper-reactivity to Cx. Those effects required the presence
of PAF-acether in the platelet suspension and persisted when transformation of PAF-acether
into its recognized metabolite alkyl-acyl-glycerophosphorylcholine was inhibited.
The ADP and thromboxane-independent activation of rabbit platelets by low and medium
concentrations of Thr may be accounted for by platelet formation of PAF-acether, but
overall the contrasting effects of platelet desensitization to PAF-acether on responsiveness
to Thr and to Cx suggest that the third pathway of aggregation requires other explanations.
Key words
ADP - Convulxin - PAF-acether (platelet-activating factor) - Thromboxane - Thrombin
- Rabbit platelets
