High impact information on ADORA2A

• We hypothesized that a selective adenosine A2A receptor agonist would induce coronary vasodilatation appropriate for pharmacological stress imaging, without evoking adenosine receptor-mediated side effects [1].
• Pharmacological stress thallium scintigraphy with 2-cyclohexylmethylidenehydrazinoadenosine (WRC-0470). A novel, short-acting adenosine A2A receptor agonist [1].
• Reduction of infarct size and postischemic inflammation from ATL-146e, a highly selective adenosine A2A receptor agonist, in reperfused canine myocardium [2].
• Either saline (Control, n=8), Ado (140 microg/kg/min, n=8) or CGS21680, an adenosine A2A receptor analogue, (0.2 microg/kg/min, n=7) were infused during the first 2 h of reperfusion [3].
• In conclusion, the present study suggests that inhibition of apoptosis by Ado at reperfusion involves alterations in anti-apoptotic Bcl-2 and pro-apoptotic Bax proteins and neutrophil accumulation, primarily mediated by an adenosine A2A receptor. * P<0.05 v Control group [3].

Biological context of ADORA2A

• Graded doses of CGS21680 (1-300 nmol/kg), a selective adenosine A2A receptor agonist, produced dose-dependent increases in the secretory rate of pancreatic juice, with a maximum effect at approximately 30 nmol/kg [4].

Anatomical context of ADORA2A

• We now demonstrate the existence of this antagonistic interaction in a fibroblast cell line (Ltk-) stably transfected with the human dopamine D2 (long-form) receptor and the dog adenosine A2A receptor cDNAs (A2A-D2 cells) [5].

Associations of ADORA2A with chemical compounds

• DMPX (5-50 nmol/kg), a weak adenosine A2A receptor antagonist, caused a progressive parallel shift to the right in the dose response curve for CGS21680-induced pancreatic secretion without changes in the maximal response [4].

References