Author(s): Schaper W
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Abstract Dipyridamole, developed almost half a century ago, acts by inhibiting nucleoside transport, which increases adenosine levels leading to inhibition of platelet aggregation and vasodilatation mainly in the coronary tree. It is a vaso-protective drug with proven efficacy in the prevention of strokes. Adenosine receptor 2 inhibitory purines, ubiquitously available in food and drink, inhibit the vasomotor effects of dipyridamole but not its action on platelet aggregation. This and the slow build-up of blood levels of dipyridamole after oral application may explain why incidents of drug-induced angina ("coronary steal") were never reported in the prevention trials. The prevention of arterial thrombosis and the positive remodeling of the arterial system (arteriogenesis) by elevated blood flows suggest that dipyridamole may be able to halt the progression of organ manifestations of atherosclerosis. Clinical trials for the secondary prevention of vascular occlusions in other vascular beds should be encouraged.
This article was published in Cardiovasc Drugs Ther
and referenced in Journal of Addiction Research & Therapy