Earlier studies in experimental hypertension have shown that acute hypertension leads to wall remodelling, which, in general, aims in restoring mean wall stress to control levels. This postulate has not been yet thoroughly studied, mainly because precise knowledge of stresses acting on each wall constituent and in all parts of the wall is still a difficult task. This requires a constituent-based modelling and analysis of the arterial wall. The three-dimensional biomechanical behavior of the vascular wall is best described by means of strain energy functions, which allow for the analysis of stresses over a wide range of deformations. The Zulliger et al. model developed by our group uses a strain energy function, which accounts for the constituents and structural properties of the wall (i.e., collagen, elastin and vascular smooth muscle as well as a statistical description for collagen engagement). The Zulliger et al. model was subsequently challenged by the work of Roy et al., which showed that significant residual stresses are released when the arterial wall is decellularized, suggesting an in-series arrangement of the VSM with elastin. The in-series elastin would be in tension, whereas the in-parallel elastin would be in compression. Upon VSM disruption, the in-series elastin cannot bear tension anymore and thus the compressed elastin expands relieving the additional residual strains. Treatment with Cytochalassin D partially destroys stress fibres and disengages the VSM cytoskeleton, leading to further release of residual stresses and to a more compliant wall, all being consistent with the model of Roy et al.