The deterioration of arterial elasticity is caused by a variety of mechanisms, including the development of endothelial dysfunction and the impairment of vasodilation mechanisms via endothelium-derived nitric oxide (NO) and the absence of ETB receptors, which increase the plasma endothelin-1 concentration because these receptors contribute to endothelin-1 destruction [35, 36]. Here, EDN1 is linked to endothelial dysfunction.