One of the main pathogenetic pathways of endothelial dysfunction development is an increased formation and biological activity of the powerful vasoconstrictor and proinflammatory peptide endothelin (ET-1) [2], which mediates own effects via two pharmacologically distinguishable receptor subtypes, endothelin A (ETA) and endothelin B (ETB) receptors, respectively [3]. Here, EDN1 is linked to endothelial dysfunction.