Chronic activation of the sympathetic nervous system (SNS) and rennin-angiotensin-aldosterone system (RAAS) contributes to hypertension by excessive production of catecholamines, such as noradrenaline and adrenaline, angiotensin II, and aldosterone, which stimulate adrenoceptors, angiotensin II receptor type 1 (AT1), and mineralocorticoid receptors to increase vascular tone, renal sodium and water reabsorption and heart rate. This evidence concerns the gene AGTR1 and hypertensive disorder.