EETs, as endothelium–derived hyperpolarizing factor, stimulate large-conductance Ca2+ – activated potassium channels (KCa++) mediating nitric oxide and prostaglandin independent vasodilation that opposes the vasoconstrictor actions of angiotensin II (Ang II) and through epoxygynase pathways provide significant influence in cardiovascular disease [25, 26, 27, 46]. This evidence concerns the gene AGT and cardiovascular disorder.