In spontaneously hypertensive rats (SHR) at an early stage of hypertension, cardiac mitochondria showed a lower respiratory control ratio and higher serum lipid peroxidation (TBARS) than normotensive WKY controls, alongside reduced SOD and GPx activity. Uridine at 30 mg/kg left blood pressure unchanged but raised complex IV and V subunit levels and returned mitochondrial H2O2 generation to control values. It did not significantly shift SOD, GPx or catalase activity, nor mitoKATP channel subunits.
This evidence comes entirely from rats, so it carries no direct implication for human supplementation. The pattern is still instructive: uridine appears to lower reactive oxygen species at the source, by adjusting electron transport and ATP synthase components, rather than by boosting antioxidant enzymes. That distinction matters because broad antioxidant supplements have repeatedly failed in human cardiovascular trials. Targeting mitochondrial ROS production is a more plausible route, yet the paper offers no cardiac outcome data such as hypertrophy, fibrosis or function to show the mitochondrial changes translate into protection. Group sizes, treatment duration and sex are not stated in the abstract, and the lower respiration rate after uridine could reflect reduced mitochondrial capacity as easily as improved efficiency. Uridine has a history in animal models of ischemia and metabolic stress, and it is sold as a supplement, but human cardiovascular trials are lacking. Editorially, this is an incremental, hypothesis-generating preclinical finding. It offers no basis for self-treating hypertension, and blood pressure control through established means remains the priority.