Adenosine receptors pharmacology and rapiscan
Adenosine is produced locally under conditions of uncommon stress and has been referred to as the retaliatory metabolite. 1,2 In the heart, the A2A adenosine receptor is responsible for coronary vasodilation resulting in an increase in coronary blood flow and is believed to cause sympathoexcitation, wheras the A1 receptor slows arterioventricular (AV) and sinoatrial (SA) nodal conduction.2-5 In the lung, the A2B and A3 adenosine receptors have been implicated in the pathophysiology of bronchoconstriction in susceptible individuals (i.e., asthmatics).2 ![]() Regadenoson is a low affinity agonist (Ki ≈ 1.3 μM) for the A2A adenosine receptor, with at least 10-fold lower affinity for the A1 adenosine receptor, and very low, if any, affinity for the A2B and A3 adenosine receptors.6 Despite low affinity for the A2A adenosine receptor, in animal models, regadenoson has high potency for increasing coronary conductance (an indirect measure of coronary blood flow velocity) and selectivity (≥ 215-fold) for increasing coronary conductance (A2A-mediated response) relative to slowing of cardiac AV nodal conduction (A1-mediated response) as measured by AV conduction time.6 Due to differences in receptor density and the selectivity of Rapiscan, in animals regadenoson was shown to preferentially increase blood flow in coronary relative to peripheral (forelimb, brain, pulmonary) arterial vascular beds.6,7 In a human clinical trial, Rapiscan was shown to cause a rapid increase in blood flow, which is sustained for several minutes - sufficient for radionuclide myocardial extraction.6,8 References
|