Revitalizing cardiac health in chronic renal failure: the synergistic effects of angiotensin-converting enzyme inhibitors and vitamin C in modulating nitric oxide and left ventricular hypertrophy.

Abstract

The inducible form of nitric oxide (iNOS) is induced by cytokines and endotoxins. The cardiac-protective effects of nitric oxide (NO) secreted by endothelial NOS are dependent on arginine. Arginine production occurs mainly within the organism, with the kidneys playing a key role in its synthesis and the elimination of asymmetric dimethylarginine (ADM). In the present study the relationship between iNOS, ADMA and left ventricular hypertrophy in chronic kidney disease (CKD) patients and the effect of treatment with angiotensin converting enzyme inhibitor (ACEI) associated with vitamin C (Vit C) were investigated. A longitudinal observational study was conducted on 153 patients with CKD. We studied the correlation between the mean values of iNOS and ADMA in CKD patients and its relationship with left ventricular hypertrophy and the benefit of treating these patients with an associated ACEI and Vit C. The mean age of the patients was 58.85 ±12.75 years. The mean values of iNOS and ADMA were 63.92 ± 0.59 μmol/l and 16.77 ±0.91 μmol/l, respectively. These values increased significantly with the degradation of the renal function (p < 0.05). A significant positive correlation was found between the left ventricular mass index (LVMI) and the two markers, ADMA (0.901 and p = 0001) and iNOS (0.718 and p = 0.0001). After 2 years of treatment with Vit C and ACEI, a significant decrease in LVMI was observed. NO secreted by the iNOS system and ADMAs initiates cardiac remodeling to lead to left ventricular hypertrophy and cardiac fibrosis. ACEIs increase the expression and activity of eNOS and decrease iNOS. Vit C prevents oxidative damage by scavenging ROS species and reagents nitrogen while. iNOS and ADMA accelerate cardiac aging. We conclude that ACEIs combined with Vit C may improve heart health and limite left ventricular hypertrophy in CKD patients.