Demonstrates that products of sodium arachidonate metabolism can directly induce platelet aggregation independently of ADP release.
Animal data implicate arachidonate metabolites in ADP-independent aggregation; hypothesis-generating for COX pathways and leaves open human translation.
Sodium arachidonate causes shape change and aggregation of rabbit or human platelets that have been washed and then degranulated by treatment with thrombin. Since these platelets do not contain releasable adenosine diphosphate (ADP) and the aggregation is not inhibited by the creatine phosphate-creatine phosphokinase system, sodium arachidonate must be able to cause aggregation that is independent of the release of ADP. Since aggregation of these platelets induced by sodium arachidonate is inhibited by acetylsalicylic acid or indomethacin, it seems likely that products (such as prostaglandin G2) formed from sodium arachidonate are responsible for aggregation. Thus, sodium arachidonate-induced shape change and aggregation of platelets may be caused (i) by the release of ADP by products of sodium arachidonate metabolism and (ii) directly by the products of sodium arachidonate metabolism, independently of released ADP.
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Kinlough-Rathbone et al. (1976) studied this question.
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