ADORA2B binds Ade-Rib

Adenosine receptors A2a and A2b (ADORA2A and ADORA2B) bind extracellular adenosine (Ado-Rib) and are believed to play a role in regulating myocardial oxygen consumption and coronary blood flow (Peterfreund 1996). The A2A receptor is responsible for regulating myocardial blood flow by vasodilation of the coronary arteries, which increases blood flow to the myocardium, but may lead to hypotension. Just as in A1 receptors, this normally serves as a protective mechanism. A2B receptor work (Pierce KD et al, 1992) has lagged behind research in the other adenosine receptors.<br>Both ADORA receptors mediate their actions by coupling with the G protein alpha s subunit which activates adenylyl cyclase and increases intracellular cAMP concentrations. In surfactant physiology, the receptor:adenosine complex positively regulates surfactant export from lamellar bodies. (Cooper JA et al, 1995; Linden J et al, 1999). Adenosine deaminase (CECR1, ADA2) degrades extracellular adenosine (Ade-Rib), reducing or neutralising the positive regulatory effect of adenosine in surfactant export.

腺苷受体A2a和A2b（ADORA2A和ADORA2B）与细胞外腺苷（Ado-Rib）结合，据信在调节心肌氧消耗和冠状动脉血流（Peterfreund 1996）中发挥着作用。A2A受体通过扩张冠状动脉，增加心肌血流量来调节心肌血流，但可能导致低血压。正如A1受体一样，这通常作为一种保护机制。A2B受体的研究（Pierce KD et al, 1992）在其它腺苷受体研究中相对滞后。ADORA受体通过与其G蛋白αs亚单位偶联介导其作用，该亚单位激活腺苷酸环化酶并增加细胞内cAMP浓度。在表面活性剂生理学中，受体：腺苷复合物正调节表面活性剂从层状体中的排出。（Cooper JA et al, 1995；Linden J et al, 1999）。腺苷脱氨酶（CECR1，ADA2）降解细胞外腺苷（Ade-Rib），降低或中和腺苷在表面活性剂排出中的正调节作用。