Effects of ionic substitution on [Ca2+]i rises evoked by thrombin and PAF in human platelets.
We have investigated the effects of substituting extracellular Na+ by choline or K+ on responses of quin2- and fura-2-loaded human platelets to thrombin and platelet-activating factor (PAF). Na+ substitution by choline did not affect the extent of the rise in [Ca2+]i evoked by either agonist. The response to thrombin, but not PAF, was slightly slowed. High K+ did not activate the cells, but the rises in [Ca2+]i evoked by both agonists were slowed and reduced. Shape change evoked by both agonists was little affected by either substitution. Aggregation evoked by PAF was reduced in high K+ but unaffected in choline. Thrombin-induced aggregation was unaffected by either substitution, even when the rise in [Ca2+]i was markedly reduced. The results suggest that the mechanism which generates Ca2+ fluxes in platelets is not voltage-dependent; but high K+ appears to interfere with the influx mechanism.
D001792:Blood Platelets / Q000187:drug effects*; D002118:Calcium / Q000097:blood*; D002794:Choline / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007700:Kinetics; D010972:Platelet Activating Factor / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects; D012964:Sodium / Q000494:pharmacology; D013917:Thrombin / Q000494:pharmacology*
D010972:Platelet Activating Factor; D012964:Sodium; D013917:Thrombin; D002794:Choline; D002118:Calcium