Involvement of the NO, PGI₂, and Ado receptor in the inhibition of ADP-induced platelet aggregation by AMP preincubated on HUVECs.

HUVEC-containing wells and blank wells were treated with (A) 0.1-10 mmol/L L-NAME or (B) 0.01-1 mmol/L aspirin. After washing, the wells were incubated with 30 μmol/L AMP at 37°C for 15 minutes. The inhibitory activity of the AMP buffer preincubated on HUVECs against ADP-induced platelet aggregation was examined. ● and ○ denote the AMP buffer preincubated on HUVECs and blank wells, respectively. The concentrations of NO (panel A, ▴) and PGI₂ (panel B, ▴) in the buffer incubated on HUVECs are also shown. The results are the mean ± SD of 3 separate experiments. (C) HUVEC-containing wells and blank wells were treated with 30 μmol/L AMP at 37°C for 15 minutes. CSC, a selective A_2a receptor antagonist, was added with the AMP-containing buffer preincubated on HUVECs to PRP in 10-fold dilution immediately before activation by ADP (final concentration, 2 μmol/L). The results are the mean ± SD of 3 separate experiments.