Blood flow properties are dictated by RBC, their deformation, and the hydrodynamic interactions between cells and with blood vessel walls. The inner surface of blood vessels is covered with a monolayer of endothelial cells (EC). RBCs convert shear stress into a biochemical response, resulting in the release of ATP, and calcium (Ca) and Nitric Oxide (NO) signaling of ECs. Endothelial dysfunctions are known to lead to a number of blood and vascular disorders, such as thrombosis, atherosclerosis, and diabetes mellitus. ATP is not only released by EC, but also by RBC under the action of shear stress. The purpose of present work is to understand how the cell dynamics influence the signaling process. In previous study, we have already proposed and numerically solved the first model of the coupling of RBC and ATP release. Using this model, we found a non-monotonous relation between ATP release per cell and hematocrit. Conditions for maximal ATP release per cell are identified, which depend on vessel size and hematocrit. In recent work, stable ATP patterns are observed in both microchannel network and mesentery-like vessel network. The increase of ATP concentration around bifurcation apex indicates potential activation of calcium signaling and regulation of vessel diameter.