Rosuvastatin Increases Extracellular Adenosine Formation in Humans In Vivo

• DOI: 10.1161/atvbaha.108.179622
• Publication Date: 2009-04-10T02:14:42Z
• Authors: Patrick Meijer; Wim J.G. Oyen; Douwe Dekker; Petra H.H. van de...; Constatijn W. Wou...; Otto C. Boerman; Gert Jan Scheffer; Paul Smits; Gerard A. Rongen
• Keywords: Adenosine receptor antagonist; Dipyridamole

Objective— Statins may increase extracellular adenosine formation from monophosphate by enhancing ecto-5′-nucleotidase activity. This theory was tested in humans using dipyridamole-induced vasodilation as a read-out for local formation. Dipyridamole inhibits the transport of into cytosol resulting increased and subsequent vasodilation. In addition, we studied effect statin therapy forearm model ischemia-reperfusion injury. Methods Results— Volunteers randomly received rosuvastatin or placebo double-blind parallel design (n=21). The vasodilator response to intraarterial dipyridamole determined absence presence antagonist caffeine. During separate visit nitroprusside established. healthy men were divided 3 groups receive either (n=10), (n=22), combined with intravenous caffeine (n=12). Subsequently, volunteers performed ischemic exercise. At reperfusion, Tc-99m–labeled annexin A5 infused intravenously scintigraphic images acquired, providing an early marker cell Rosuvastatin treatment significantly dipyridamole, which prevented did not influence sodium indicating specific interaction between does result on clearance nor adenosine-receptor affinity efficacy. tolerance injury, attenuated Conclusions— increases formation, provides protection against injury vivo. Therefore, statins interact synergistically.