Taken together, it can thus be concluded that, although aneurysmal and non‐aneurysmal 4‐week AngII‐treated mice showed similar underlying changes in aortic physiology (i.e., endothelial dysfunction, heightened α1‐adrenergic contractility, and altered VSMC calcium signaling), the biomechanics of the aorta were dissimilarly affected and in a markedly pressure‐dependent fashion, due to extreme passive aortic stiffening in aneurysmal AngII‐treated mice. This evidence concerns the gene AGT and endothelial dysfunction.