FIGURE 3.

Effect of purinergic receptor inhibition on endothelial function of aortas in recipient rats transfused with rat RBCs. Effect of the A1R antagonist DPCPX, the P2X₇R antagonist A438079 and the P2Y₆R antagonist MRS2578 on EDR in aortas of rats transfused with GK RBC (A: n = 6, B: n = 8, C: n = 6). Schematic summary of the present study (D): Dysfunctional RBCs of T2D alter vascular A1R and P2X₇R but not P2Y₆R accounting for endothelial dysfunction. Dashed boxes represent earlier findings where there are decreased nitric oxide (NO) bioavailability, increased reactive oxygen species (ROS) formation/release and impaired release of ATP from RBCs of T2D that break the balance between NO bioavailability and ROS in the endothelium (Pernow et al., 2019). Signaling in blue color represents the hypothesized mechanisms that the increased formation of ROS derived from RBCs may stimulate ATP release in other (endothelial) cells than RBCs to activate P2X₇R in endothelium. Together with the subsequent degradation product adenosine, vasoconstrictor A1R and P2X₇R are activated in T2D accounting for endothelial dysfunction. Values are mean ± SD. *p < 0.05 effect of antagonist. Ado: adenosine.