Structural adaptation in arterioles is part of normal vascular physiology but is also seen in disease states such as hypertension. Smooth muscle cell (SMC) activation has previously been shown to be central to microvascular remodeling. We hypothesize that in a remodeling process driven by SMC-activation, stress sensitivity of the vascular wall is a key element in the process of achieving a stable vascular structure. We address the question whether the adaptive changes seen in arterioles under different conditions can arise through a common mechanism: remodeling in a stress-sensitive wall, driven by a shift in SMC-activation. We present a simple dynamic model and show that structural remodeling of vessel radius, by a rearrangement of the wall material around a lumen of a different diameter and driven by differences in SMC-activation, can lead to vascular structures similar to those observed experimentally under various conditions. The change in structure simultaneously leads to uniform levels of circumferential wall stress and wall strain despite differences in transmural pressure. A simulated vasoconstriction caused by increased SMC-activation leads to inward remodeling, whereas outward remodeling follows relaxation of the vascular wall. The results are independent of the specific myogenic properties of the vessel. The simulated results are robust to parameter changes and hence may be generalized to vessels from different vascular beds.