Figure 3.

Abacavir interrupts NO‐mediated inhibition of platelet activation. Platelet aggregation was monitored by light transmission aggregometry in response to 3‐μM ADP. Platelets were preincubated for 3 min with 5 μM SNAP (a,b), 5‐μM forskolin (c), or vehicle control (0.5% DMSO). 1H‐[1,2,4]oxadiazolo[4,3‐a]quinoxaline‐1‐one (ODQ; 20 μM) was applied to assess the contribution of soluble GC to the SNAP‐mediated inhibition (a,b), while the adenylate cyclase pathway was probed by SQ22536 (SQ; 100 μM; c). The effect of CBV‐TP (a,c; 50 μM) or tenofovir (TFV: b,c; 50 μM) on NO‐ (a,b) or adenylate cyclase‐mediated (c) platelet inhibition was assessed. Data are representative of seven (a,b) and five (c) independent experiments. *P < 0.05, significantly different as indicated; two‐way ANOVA