Flow-induced dilation of blood vessel is the result of a series of bioreaction in vascular endothelial cells(VEC). Shear stress change by blood flow in human artery or vein is sensed by the mechanoreceptor and responsible for such a chain reaction. The inositol(1,4,5)-triphophate($IP_3$) is produced in the first stage to elevate permeability of the intercellular membrane to calcium ions by which the cytosolic calcium concentration is consequently increased. This intracellular calcium transient triggers synthesis of EDRF and prostacyclin. The mathematical model of this VEC calcium dynamics is reproduced from the literature. We then use the Computational Fluid Dynamics(CFD) technique to investigate the blood stream dictating the VEC calcium dynamics. The pulsatile blood flow in a stenosed blood vessel is considered here as a part of study on thrombogenesis. We calculate the pulsating shear stress (thus its temporal change) distributed over the stenosed artery that is implemented to the VEC calcium dynamics model. It has been found that the pulsatile shear stress induces larger intracellular $Ca^{2+}$ transient plus much higher amount of EDRF and prostacyclin release in comparison with the steady shear stress case. It is concluded that pulsatility of the physiological shear stress is important to keep the vasodilation function in the stenosed part of the blood vessel.