Fig. 2

Trajectory-dependent [Ca²⁺]_c flux occurs independent of platelet adhesion receptor engagement and amplification loops. A Ca²⁺ sampling along T14 following treatment of reconstituted blood platelets with α-GPIb/V/IX blocking antibody AK2 (5 μg/mL) or α-α _IIbβ₃ blocking antibody c7E3 Fab (Reopro©; 1 μg/mL). DMSO—vehicle control (N = 9 experiments); AK2—GPIb/V/IX blockade (N = 3 experiments); c7E3Fab (ReoPro)—integrin α_IIbβ₃ blockade (N = 5 experiments). B Ca²⁺ sampling along T14 following treatment of reconstituted blood platelets with amplification loop inhibitors for 10 min. DMSO—vehicle control (N = 11 experiments); Indomethacin (10 μM) to inhibit COX1 (N = 3 experiments); MRS2179 [100 μM] to inhibit P2Y1 (N = 3 experiments); 2-MeSAMP [10 μM] to inhibit P2Y12 ADP dependent signaling (N = 5 experiments); ALB—all inhibitors combined (N = 3 independent experiments)