The peripheral administration of adenosine agonists can produce pain inhibitory effects due to adenosine A1 receptor activation, and pain facilitatory effects due to adenosine A2 and A3 receptor activation. Pain facilitatory effects for A2‐like receptors result from interactions with endogenous mediators like 5‐hydroxytryptamine. Both pain facilitation and edema resulting from local administration of A3 agonists results from release of histamine and 5‐hydroxytryptamine from mast cells. Local administration of adenosine kinase, but not adenosine deaminase inhibitors, produces a local antinociception, but no pronociception occurs at higher doses due to systemic (probably spinal) pain‐suppressing mechanisms being recruited. In the spinal cord, adenosine A1 receptors produce antinociception. Inhibition of adenosine kinase, but not adenosine deaminase, also produces antinociception, and exhibits a greater separation from motor effects. Adenosine A1 receptor agonists, as well as inhibitors of adenosine kinase, exhibit the potential for development as analgesic agents, both as local formulations, as well as systemically active agents. In both instances, a sufficient separation from adverse effects will be required. Drug Dev. Res. 45:304–311, 1998. © 1998 Wiley‐Liss, Inc.

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