Interaction between platelet-aggregating response and vasoconstrictive response to platelet activating factor

It is very important to know under medical treatment which kinds of platelet agonists participate in abnormal platelet-blood vessel interactions. The present study, focusing on platelet activating factor (PAF) was undertaken in an attempt to investigate its action on platelet aggregating response and vasocontractile response to noradrenaline (NA-R). We used autologous platelets and isolated perfused arterial segments from Japanese white rabbits. Firstly, typical tracings of platelet aggregating response to PAF were increased in a dose-dependent fashion, which remained constant and long-lasting. Secondly, noradrenaline (NA) at 5 to 25 ng elicited an initially augmented response in the presence of platelet rich plasma (PRP) with PAF, followed by gradually attenuated responses. Based on the light transmission intensity, platelet aggregation did not seem to be directly or strictly linked to vasocontractile response. Pretreatment with either dibutyryl cyclic AMP (DBcAMP) or indomethacin (IM, a cyclo-oxygenase inhibitor) clearly caused reductions in NA-R as well as platelet aggregation in the presence of PRP with collagen, whereas platelet aggregation and NA-R in the presence of PRP with PAF were scarcely influenced by pretreatment with either DBcAMP or IM. Thus, it seems reasonable to conclude that, in contrast to the response to collagen, platelet aggregation response to PAF was almost indifferent to the adenylate cyclase-cyclic AMP system and the cyclo-oxygenase metabolic pathway.