Jacobsen JC, Mulvany MJ, Holstein-Rathlou N-H. A mechanism for arteriolar remodeling based on maintenance of smooth muscle cell activation. Am J Physiol Regul Integr Comp Physiol 294: R1379-R1389, 2008. First published January 9, 2008 doi:10.1152/ajpregu.00407.2007.-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 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 whether the adaptive changes 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 the vessel radius by 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 in the face of parameter changes and, hence, may be generalized to vessels from different vascular beds. essential hypertension; microcirculation; eutrophic remodeling VESSELS OF THE MICROCIRCULATION must continuously meet the changing demands of the tissues. On short time scales, vascular diameter and, hence, tissue perfusion are regulated by variation in smooth muscle cell (SMC) activation. On longer time scales, resistance vessels adapt structurally to maintain dimensions optimal for acute flow regulation. In microvascular networks in vivo, such adaptation depends on a complex interplay between various stimuli, including pressure, shear stress, and metabolic status of the tissue (38).As noted six decades ago by Folkow and co-workers (15), in human essential hypertension, resistance vessels develop a reduced lumen size and an increased wall thickness. These changes are apparently caused by redistribution of the wall material around a smaller lumen, i.e., inward eutrophic remodeling (33), and allow the vessel to operate at normal or near-normal levels of activation, despite increased pressure (14).Another example of structural adaptation is the surprising observation by Bakker et al. (7) that, in unbranched segments of first-order rat cremaster arterioles, structural diameter does, in fact, increase distally along the vessel. This increase in diameter is not associated with an increase in wall transsectional area. Rather, analogous ...