Adenosine, a byproduct of ATP, produces its beneficial effects by binding to specific cell surface proteins termed adenosine receptors. Three subtypes of adenosine receptors have been described to date - A1, A2 and A3 subtypes. These receptor subtypes are encoded by different genes and show distinct tissue distribution and pharmacological profiles.

   A major goal of this laboratory is to understand the mechanism(s) by which adenosine produces vascular smooth muscle relaxation. Initial evidence suggests that relaxation is dependent, in part, on an intact vascular endothelium. The presence of a novel A3 adenosine receptor on endothelial cells suggest a role of these receptors in the vasorelaxation property of adenosine. Current research efforts are geared towards understanding whether activation of these receptors on endothelial cells can increase the release of endothelium derived relaxing factor (EDRF), leading to smooth muscle relaxation. We are also interested in whether the function of these receptors are altered in hypertension.

   We have recently demonstrated that the adenosine receptors on mast cells is exclusively of the A3 subtype. Activation of this receptor facilitates the release of allergic mediators from mast cells. The focus of this study is to understand the biochemical basis of A3AR-stimulated release of these mediators and to determine how antiallergic and antiasthmatic drugs can regulate the function on the these receptor proteins. Furthermore, we are interested in whether increased expression of these receptors can predispose individuals to asthmatic attacks.