A₁ antagonism in asthma: better than coffee?
J. Clin. Invest. Stephen L. Tilley, et al. 115:13 doi:10.1172/JCI24009 [Go to this article.]

Figure 1
Extracellular adenosine is produced predominantly by the metabolism of ATP released from cells. ATP is sequentially dephosphorylated by a series of membrane-bound and soluble ectonucleotidases to produce adenosine. Adenosine can act at 4 different 7-transmembrane, G-protein–coupled receptors present on the surfaces of both infiltrating leukocytes and resident parenchymal cells. While both proinflammatory and anti-inflammatory signals can be sent depending on the specific adenosine receptor activated, adenosine produces a net proinflammatory effect in the asthmatic airway. ADA is the primary catabolic enzyme for adenosine, and its absence in ADA-deficient mice results in marked elevations of extracellular adenosine. Elevations of extracellular adenosine are present in the asthmatic lung due to both increased release of ATP from cells and inhibition of ADA by local hypoxia. E-NPPs, ectonucleotide pyrophosphatase/phospho-diesterases; AP, alkaline phosphatase; NTPDases, ectonucleoside triphosphate-diphosphohydrolases.