oxLDL modulates cGMP-mediated inhibition of platelet aggregation and arrest under conditions of flow. (A) Washed human platelets (3 × 10⁸ platelets/mL) were incubated with 8-pCPT-cGMP (50 µmol/L) for 2 minutes alone or with nLDL or oxLDL (50 μg/ml) for 15 minutes followed by 8-pCPT-cGMP (50 µmol/L) for 2 minutes. Thrombin-stimulated aggregation was then measured under constant stirring (1000 rpm) at 37°C for 3 minutes. Aggregation was recorded for 3 minutes. (i) Representative aggregation traces. (ii) Percent inhibition of thrombin induced aggregation by cGMP is presented as mean ± SD (n = 4, *P < .05 compared with absence of oxLDL). (B) As in panel A, except platelets were incubated with gp91ds-tat or its scrambled control (both 2 µmol/L) prior to the addition of oxLDL. (i) Representative aggregation traces. (ii) Percent inhibition of thrombin induced aggregation by cGMP is presented as mean ± SD (n = 4). *P < .05. (C) As in panel A, except WT and NOX2^−/− murine platelets were treated with oxPC_CD36 or PAPC (5 µmol/L) for 15 minutes followed by 8-pCPT-cGMP (50 µmol/L) for 2 minutes. (i) Representative aggregation traces are shown. (ii) Percent inhibition of thrombin induced aggregation by cGMP is presented as mean ± SD (n = 3). *P < .05 compared with the absence of oxPC_CD36.