Background:

Dipyridamole (Persantine) is a phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells.Target: Phosphodiesterase (PDE)Dipyridamole concentrations of 1 nmol/ml blood caused 90% inhibition of adenosine metabolism. Dipyridamole at therapeutic concentrations causes significant inhibition of adenosine metabolism in whole blood [1]. Dipyridamole has a dose-dependent inhibitory effect on thromboxane synthesis which was independent of aggregation. Dipyridamole also inhibited malonyldialdehyde production in response to both thrombin and arachidonic acid [2]. Dipyridamole enhances platelet inhibition by amplifying the signaling of the NO donor sodium nitroprusside. These data support the concept that enhancement of endothelium-dependent NO/cGMP-mediated signaling may be an important in vivo component of dipyridamole action [3].

参考文献:
[1]. Klabunde, R.E., Dipyridamole inhibition of adenosine metabolism in human blood. Eur J Pharmacol, 1983. 93(1-2): p. 21-6.
[2]. Best, L.C., et al., Mode of action of dipyridamole on human platelets. Thromb Res, 1979. 16(3-4): p. 367-79.
[3]. Aktas, B., et al., Dipyridamole enhances NO/cGMP-mediated vasodilator-stimulated phosphoprotein phosphorylation and signaling in human platelets: in vitro and in vivo/ex vivo studies. Stroke, 2003. 34(3): p. 764-9.