Role of the<scp>A_2B</scp>receptor–adenosine deaminase complex in colonic dysmotility associated with bowel inflammation in rats

Abstract

Under normal conditions, endogenous adenosine modulates colonic motility via A2B receptors located in the neuromuscular compartment. In the presence of colitis, this inhibitory control is impaired due to a link between A2B receptors and adenosine deaminase, which catabolizes adenosine, thus preventing A(2B) receptor activation.