At the molecular level, the elevated ROS level in RVLM was attributed by an increase in gp91phox subunit of the NADPH oxidase and downregulation of the antioxidant SOD2, suppression of PGC-1α and TFAM expression, together with decrease in mitochondrial DNA copy number, events known to underpin sympathoexcitation in animal models of hypertension [18–23]. This evidence concerns the gene TFAM and hypertensive disorder.