ABSTRACTObjective:To test the hypothesis that terminal arteriolar remodeling that is stimulated by elevated levels of circumferential wall stress (σθ) will proceed in a network pattern that gives rise to new arcade arterioles.Methods:A network model of two interconnected skeletal muscle arterio‐capillary‐venous units that incorporated diameter‐ and hematocrit‐dependent blood viscosity was constructed. After computing the control values for wall shear stresses (τij) and σθij, a stimulus was provided by dilating the arterioles and raising input pressure. Wall shear stresses and σθijwere then recomputed. The diameters of transverse arteriolar segments with σθijgreater than a σθthreshold were increased by an amount that was dependent on the original diameter and the difference between σθand the σθthreshold. Capillaries with an intraluminal pressure greater than a specified threshold were converted to terminal arterioles. Separate simulations in which remodeling was stimulated by elevated levels of τijwere also performed for comparison.Results:Arterialization patterns from simulations of σθijstimulated arteriolar remodeling were representative of those seenin vivowith arterialization of back‐connection capillaries leading to arcade arteriole formation. Simulations based on similar rules for τijyielded arterio‐venous shunts, which are rarely seenin vivo, but no arcade arterioles.Conclusion:The simulations presented here are consistent with the hypothesis that arteriolar remodeling is stimulated by increased levels of circumferential wall stress and that new arcade arteriole formation is a consequence