Besides the shortage of vasodilative action of NO itself, reduced NO availability in the renal artery is thought to stimulate renin release, followed by angiotensin II (Ang II)—aldosterone axis activation in the circulation [15] and in tissues such as the heart and aorta [16] or kidney [14,17], thus contributing to hypertension development and end-stage organ damage [15]. This evidence concerns the gene AGT and Hypertension.