Sodium arachidonate induced platelet aggregation is independent of secreted adenosine diphosphate.
Human gel-filtered platelets or platelet-rich plasma were stimulated by sodium arachidonate or by ADP in the presence of two compounds known to inhibit ADP mediated aggregation and secretion - ATP and N-ethylmaleimide. Using gel-filtered platelets and the lowest concentration of agonist necessary to elicit maximum aggregation, fifty percent inhibition of ADP-mediated aggregation required 9 microM N-ethylmaleimide or 23 microM ATP. Sodium arachidonate-mediated aggregation was significantly less sensitive; equivalent inhibition required 30 microM N-ethylmaleimide or greater than 500 microM ATP. Concentrations of both inhibitors were determined that would completely inhibit ADP-induced aggregation yet would not completely prevent sodium arachidonate-induced aggregation. Furthermore, this concentration of N-ethylmaleimide could not be overcome by up to 500 microM ADP, demonstrating that the observed arachidonate-induced aggregation was not due to the effects of a small amount of secreted ADP acting at the platelet surface. Therefore, aggregation of human platelets induced by arachidonic acid can occur by a mechanism that is independent of secreted ADP.
D000227:Adenine Nucleotides / Q000032:analysis; D000244:Adenosine Diphosphate / Q000037:antagonists & inhibitors / Q000378:metabolism* / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000494:pharmacology; D001095:Arachidonic Acids / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D005033:Ethylmaleimide / Q000494:pharmacology; D005110:Extracellular Space / Q000032:analysis; D006801:Humans; D010974:Platelet Aggregation / Q000187:drug effects*
D000227:Adenine Nucleotides; D001095:Arachidonic Acids; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D005033:Ethylmaleimide