Prevention of pressure natriuresis deterioration by dietary coenzyme Q10: Role of mitochondrial preservation in reduced renal mass and high-sodium diet

Abstract

Moderate glomerular mass reduction is emerging as a critical factor that exacerbates susceptibility to blood pressure (BP) elevation. In this way, it accounts for 40%–50% of all hypertension cases. Coenzyme Q10 (CoQ10) has antioxidative properties and anti-inflammatory response that could prevent blood pressure elevation and preserve renal functional reserve supporting the pressure natriuresis mechanism. Wistar rats underwent uninephrectomy (UNX) and were divided into four groups: G1 normal-sodium diet (NNaD); G2 high-sodium diet (HNaD4%); G3 HNaD4% with CoQ10 supplementation (200 mg/kg/day) (HNaD4%+CoQ10); and G4 NNaD with CoQ10 supplementation (CoQ10). Physiological, histological, and biochemical parameters were measured. After 45 days on a high-salt diet, G2 elevated BP while G3 did not (G2: 128±2.8 vs. G3: 119.2±3.7 mmHg, P < .05). CoQ10 effect in G3 was associated with decreased proteinuria. Creatinine clearance increased in all groups, but G3 did not. CoQ10 prevented pressure natriuresis deterioration, resulting in lower BP increases in G3 and G4. CoQ10 prevented the increase in reactive oxygen species (ROS) and systemic lipid peroxides induced by HNaD4%. In the renal cortex, it prevented mitochondrial glutathione (GSH) depletion and normalized superoxide dismutase (SOD) activity. CoQ10 improved renal morphology and ultrastructure in HNaD4%. These findings suggest a potential therapeutic role for CoQ10 in preventing the development of hypertension by protecting the pressure natriuresis mechanism and renal complications.