Arterial wall morphology depends strongly on the hemodynamic environment experienced in vivo. The mammalian heart pumps blood through rhythmic contractions forcing blood vessels to undergo cyclic, mechanical stimulation in the form of pulsatile blood pressure and flow. While it has been shown that stepwise, chronic increases in blood pressure and flow modify arterial wall thickness and diameter respectively, few studies on arterial remodeling have examined the influences that pulsatility (i.e., the range of cyclic stimuli) may have on biaxial wall morphology. We experimentally studied the biaxial behavior of carotid arteries from 8 control (CCA), 15 transgenic, and 21 mechanically altered mice using a custom designed mechanical testing device and correlated those results with hemodynamic measurements using pulsed Doppler. In this dissertation, we establish that increased pulsatile stimulation in the right carotid artery after banding (RCCA-B) has a strong affect on wall morphological parameters that peak at 2 weeks and include thickness (CCA=24.8±0.878, RCCA-B=99.0±8.43 μ m), inner diameter (CCA=530±7.36, RCCA-B=680±32.0μ m), and in vivo axial stretch (CCA=1.7±0.029, RCCAB= 1.19±0.067). These modifications entail stress and the change in stress across the cardiac cycle from an arterial wall macro-structural point of view (i.e., cellular and extracellular matrix) citing increases in collagen mass fraction (CCA=0.223±0.056, RCCA-B=0.314±0.011), collagen to elastin ratio (CCA=0.708±0.152, RCCA-B=1.487±0.26), and cross-sectional cellular nuclei counts (CCA=298±58.9, RCCA-B=578±28.3 cells) at 0, 7, 10, 14, and 42 post-banding surgery. Furthermore, we study the biomechanical properties of carotid arteries from a transgenic mouse of Marfan Syndrome. This arterial disease experiences increased pulse transmission and our findings indicate that alterations occur primarily in the axial direction. The above results are all applied to a predictive biaxial model of Cauchy stress vs. strain.