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Since the late 1920s, the importance of the physiological role of adenosine triphosphate (ATP) and its metabolites, mainly adenosine, has been clear. In 1970, strong evidence now suggests ATP as a neurotransmitter in nonadrenergic, noncholinergic (NANC) nerves supplying the gut. Initially, the hypothesis of purinergic transmission encountered some resistance, however, this concept is now widely accepted and purines are considered powerful extracellular messengers in peripheral and central nervous system and to non-neuronal cells, including immune, and inflammatory cells. Implicit in the purinergic hypothesis was the presence of purinoceptors. The first evidence for the existence of adenosine receptors, responsible for the physiological effects of adenosine, was only published in the beginning of the 1970s. Through‐ out the 1990s and 2000s adenosine receptors were cloned, and the mechanisms of signal transduction mediated by these receptors were described. Currently, it is well known that adenosine activates four G protein-coupled receptors named A1, A2A, A2B and A3. The A1 and A3 receptors preferentially interact with members of the Gi/o family of G proteins, lowering the intracellular levels of cyclic adenosine monophosphate (cAMP), whereas the A2A and A2B receptors interact with members of the Gs family of G proteins, elevating of intracellular cAMP.

Pharmacology of Adenosine Receptors and Their Signaling Role in Immunity and Inflammation