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Background and Purpose  In patients with myocardial infarction, ticagrelor reduces cardiovascular and sepsis-related mortality, and can cause dyspnea. It is suggested that this is caused by adenosine receptor stimulation, because in preclinical studies, ticagrelor blocks the nucleoside transporter and increases cellular ATP release. We now investigated the effects of ticagrelor on the adenosine system in humans  in vivo .    Experimental Approach  In a double-blinded, placebo-controlled cross-over trial in 14 healthy subjects, we have tested whether ticagrelor (180 mg) affects adenosine- and dipyridamole-induced forearm vasodilation, as surrogates of nucleoside uptake inhibition and adenosine formation, respectively. Also,  ex vivo  uptake of adenosine and uridine in isolated red blood cells was measured. Primary endpoint was adenosine-induced vasodilation.    Key Results  Ticagrelor did not affect adenosine- or dipyridamole-induced forearm vasodilation. Also,  ex vivo  uptake of adenosine and uridine in isolated red blood cells was not affected by ticagrelor.  In vitro , ticagrelor dose-dependently inhibited nucleoside uptake, but only at supra-physiological concentrations.    Conclusion and Implications  In conclusion, at relevant plasma concentration, ticagrelor does not affect adenosine transport, nor adenosine formation in healthy subjects. Therefore, it is unlikely that this mechanism is a relevant pleiotropic effect of ticagrelor.    Trial Registration  ClinicalTrials.gov  NCT01996735

Ticagrelor Does Not Inhibit Adenosine Transport at Relevant Concentrations: A Randomized Cross-Over Study in Healthy Subjects In Vivo