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The endothelium, composed of a single layer of endothelial cells, is the innermost lining of vessels, acting as the interface between blood and the arterial wall. “Endothelial dysfunction” is defined as reduction or loss of bioavailability of endothelial-derived nitric oxide (NO), a condition that precedes or accompanies several cardiovascular pathologies associated with aging, such as atherosclerosis. [1] [2] NO plays an important role in regulating vascular tone and maintaining vascular homeostasis as a vasodilator. Thus, we hypothesize that decreased NO production may induce collagen fiber reorientation and increased collagen production, to shift load from smooth muscle cells to the extracellular matrix, eventually leading to vascular remodeling. The aim of this project is to study the impact of NO deficiency on hemodynamic parameters, collagen content, and collagen fiber orientation during age-related vascular remodeling using a mouse model.