Proposed model of coordinated induction of ADA and CD26. In areas of ongoing inflammation and diminished oxygen supply, hypoxia coordinates the induction of endothelial ADA and CD26. Following induction of ADA mRNA, the enzyme is synthesized and released from the endothelial cell and binds to its cell-surface receptor CD26. Such increases in endothelial cell-surface ADA modulate vascular adenosine signaling during hypoxia. In general, extracellular adenosine can activate endothelial adenosine receptors. Due to increased ADA surface activity with hypoxia, adenosine is metabolized to inosine, thus terminating vascular adenosine signaling and increasing extracellular inosine concentration. Inhibition of ADA with dCF or inhibition of ADA binding to its receptor CD26 (GP120) can contribute to increasing vascular adenosine effects during acute hypoxia.