At the molecular level, angiotensin type 1 receptor (AT1R)-dependent activation of the nicotinamide adenine dinucleotide diphosphate oxidase (NADPH oxidase) signaling [18–20], suppression of endogenous antioxidants [18, 19, 21], impairment of mitochondrial biogenesis [18, 19, 22] and changes in protein expressions of NO synthase (NOS) isoforms [19, 23] have all been reported to contribute to the pathogenesis of hypertension via sympathoexcitation. This evidence concerns the gene NOS1 and hypertensive disorder.