Physiological levels of shear stress promote arterial stabilization, associated with low NF-kB and low expression of inflammatory mediators, high activation of Smad1/5 and Notch, moderate activation of eNOS and production of NO, and low cell proliferation. Flow-induced shear stress below physiological levels promotes inward remodeling in association with high activation and signaling by NF-kB, ET-1 and Smad2/3 as well as low eNOS/NO. Shear stress above physiological levels promotes outward remodeling in association with high NF-kB, higher eNOS/NO, cell proliferation and suppression of the stabilization pathways.