Endothelial calcium dynamics elicited by ATP release from red blood cells

Red blood cells (RBCs) exhibit an interesting response to hydrodynamic flow, releasing adenosine triphosphate (ATP). Subsequently, these liberated ATP molecules initiate a crucial interaction with endothelial cells (ECs), thereby setting off a cascade involving the release of calcium ions (Ca \(^{2+}\) $_{}^{2+}$ ). Ca \(^{2+}\) $_{}^{2+}$ exerts control over a plethora of cellular functions, and acts as a mediator for dilation and contraction of blood vessel walls. This study focuses on the relationship between RBC dynamics and Ca \(^{2+}\) $_{}^{2+}$ dynamics, based on numerical simulations under Poiseuille flow within a linear two-dimensional channel. It is found that the concentration of ATP depends upon a variety of factors, including RBC density, channel width, and the vigor of the flow. The results of our investigation reveals several features. Firstly, the peak amplitude of Ca \(^{2+}\) $_{}^{2+}$ per EC escalates in direct proportion to the augmentation of RBC concentration. Secondly, increasing the flow strength induces a reduction in the time taken to reach the peak of Ca \(^{2+}\) $_{}^{2+}$ concentration, under the condition of a constant channel width. Additionally, when flow strength remains constant, an increase in channel width corresponds to an elevation in calcium peak amplitude, coupled with a decrease in peak time. This implies that Ca \(^{2+}\) $_{}^{2+}$ signals should transition from relatively unconstrained channels to more confined pathways within real vascular networks. This notion gains support from our examination of calcium propagation in a linear channel. In this scenario, the localized Ca \(^{2+}\) $_{}^{2+}$ release initiates a propagating wave that gradually encompasses the entire channel. Notably, our computed propagation speed agrees with observations.