Some evidence indicates that endothelial dysfunction, resulting from impaired activity of the NO-dependent metabolic pathways, is considered to have a causative role in hypertension development, since decreased NO bioavailability promotes increase in peripheral arterial resistance, reduces renal ability to excrete sodium and increases angiotensin II (Ang II) formation via synthesis of angiotensin-converting enzyme (ACE) and Ang II type 1 receptors. Here, ACE is linked to endothelial dysfunction.