Abstract: Aim L-Arginine·L-aspartate, a double salt, has been recently reported to inhibit platelet aggregation and thrombosis, but its action mechanism is not clear yet. This study was conducted to investigate its effect on FITC-PAC-1, an anti-glycoprotein Iib/IIIa monoclonal antibody binding to activated platelets, and on correlative autacoid levels in plasma or in platelets in order to explore its potential pathway of inhibiting platelet aggregation and thrombosis. Methods Monoclonal antibody binding to activated platelets was assayed by flow cytometry; NO was assessed by colorimetric method.cAMP, TXB2 or 6-keto-PGF1α levels were assessed by radioimmunoassay. Results Gavaged 30 mg·kg-1 of L-arginine·L-aspartate increased both concentration of NO in plasma and 6-keto-PGF1α in incubated supernatant of aortic segment of rats ex vivo (P<0.05), but it did not influence cAMP content in platelets and the level of TXB2 or 6-keto-PGF1α in plasma of rats, whereas ASA significantly lowered TXB2 or 6-keto-PGF1α in plasma.Both 100 μmol·L^-1 of L-arginine·L-aspartate and ASA inhibited FITC-PAC-1 binding to activated platelets in vitro. Conclusion The increase in NO and PGI2 release from endothelial cells and consequent inhibition of platelet activation may contribute to the inhibition of platelet aggregation and thrombosis by L-arginine·L-aspartate; whereas arachidonic acid or cAMP metabolic pathway is not closely correlative with the studied effect.

Key words: L-arginine·L-aspartate, L-arginine·L-aspartate, nitric oxide, nitric oxide, PGI2, PGI2, TXA2, TXA2, cAMP, cAMP, glycoprotein IIb/IIIa monoclonal antibody, glycoprotein IIb/IIIa monoclonal antibody