Smooth muscle cells (SMCs) play a critical role in mediating mechanobiological stability in arteries [1]. To achieve this, SMCs interact with neighboring cells and with the extracellular-matrix (ECM), for instance, mechanical forces applied to the ECM are transmitted to SMCs through transmembrane receptors, activating feedback loops that restore forces on the cell to basal or homeostatic state. This work presents a multiscale finite element model of the arterial wall, incorporating individualized cells superposed onto the ECM structure using the embedded element method. This method kinematically bonds the cells (modeled as trusses) to the ECM, assuming a ”no-slip” condition [2]. For verification, we create an arterial wall model with media and adventitia. The media is subdivided in lamellar and interlamellar layers, with the cells embedded in the interlamellar layers. The model is compared against experimental inflation tests of a descending thoracic aorta [3], revealing localized high stress of ≈2-MPa at the innermost elastin lamellae, but an overall averaged arterial stress of ≈400-kPa, both when internal pressure reaches 150-mmHg. Stress analysis shows that the ECM, particularly the elastin lamellae, bears the highest stresses, while embedded cells exhibit lower stress levels, likely due to the stiffness difference between collagen/elastin and SMCs. This approach bridges cellular and organ-scale mechanics by coupling cells with ECM structure, enabling mechanobiological analysis of the arterial wall and the transmission of forces from ECM to cells. Future work will focus on simulating cell-driven aging in the arterial wall and quantify remodeling, deposition and degradation of ECM components.