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. 2018 Jan 29;118(2):369–380. doi: 10.1160/TH17-07-0530

Fig. 3.

Fig. 3

P2X1-mediated Ca 2+ responses to FcγRIIa receptor activation are resistant to NO and elevated apyrase levels, but are abolished by PGI 2 . Representative [Ca 2+ ] i responses ( A, B, D ) induced by FcγRIIa receptor activation by cross-linking of mAb IV.3 in the presence of elevated apyrase levels (3.2 U/mL), spermine NONOate (sNO; 100 μM), and prostacyclin (PGI 2 ; 500 nM). Control traces are representative of the vehicle-treated platelet samples in each panel (saline, 0.01 M NaOH and dH 2 O, respectively). P2X1 receptor desensitization was achieved by pretreatment with 600 nM α,β-meATP. ( C ) Effect of a submaximal concentration of PGI 2 (500 nM) on [Ca 2+ ] i induced by 0.03 U/mL thrombin. ( E, F ) PGI 2 (500 nM) substantially inhibited FcγRIIa-mediated ATP secretion. ( G ) Average peak [Ca 2+ ] i responses obtained in the presence of inhibitors used, compared with the average of control responses (first column).