The mechanisms for this side effect are largely unknown, although early data indicate that ticagrelor blocks adenosine reuptake through inhibition of ENT-1 by red blood cells, and it is known that intravenous adenosine infusion can cause transient dyspnea in the absence of bronchoconstriction. Another mechanism potentially increasing adenosine levels by ticagrelor consists in adenosine triphosphate (ATP) release from red blood cells. Moreover, comparison between ticagrelor and adenosine molecules suggests their similarity; Adenosine is a well-known key endogenous molecule that regulates tissue functions by activating 4 G-protein-coupled adenosine receptors: A1, A2A, A2B, and A3. Adenosine accumulates in the extracellular space in response to metabolic stress and cell damage; and elevations of adenosine are found in ischemia, hypoxia, inflammation, and trauma. Adenosine acts as cytoprotector by its anti-inflammatory, cardioprotective, cerebroprotective, antisclerotic, and antifibrotic properties, as well as by platelet inhibition and vasodilation.