Leila Azouaou, Mounir Adnane, Abedrrezak Khelfi, Henni Chader, Atmene Seba
Research Laboratory of Oxidative Stress, Kidney and Associated Complications, University Algiers 1, Faculty of Medicine, Hospital Hussein Dey, Hussein Dey, Algeria.
Department of Biomedical Sciences, Institute of Veterinary Sciences, University Ibn Khaldoun of Tiaret, Tiaret, Algeria.
Arch Med Sci Atheroscler Dis. 2023 Apr 12;8:e44-e52. doi: 10.5114/amsad/161519. eCollection 2023.
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 ( < 0.05). A significant positive correlation was found between the left ventricular mass index (LVMI) and the two markers, ADMA (0.901 and = 0001) and iNOS (0.718 and = 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.
一氧化氮（NO）的诱导型（iNOS）由细胞因子和内毒素诱导产生。内皮型一氧化氮合酶（eNOS）分泌的一氧化氮（NO）的心脏保护作用依赖于精氨酸。精氨酸的产生主要发生在生物体内，肾脏在其合成和不对称二甲基精氨酸（ADMA）的清除中起关键作用。在本研究中，我们调查了慢性肾脏病（CKD）患者中iNOS、ADMA与左心室肥厚之间的关系，以及血管紧张素转换酶抑制剂（ACEI）联合维生素C（Vit C）治疗的效果。
对153例CKD患者进行了一项纵向观察性研究。我们研究了CKD患者中iNOS和ADMA的平均值之间的相关性，及其与左心室肥厚的关系，以及用ACEI联合Vit C治疗这些患者的益处。
患者的平均年龄为58.85±12.75岁。iNOS和ADMA的平均值分别为63.92±0.59μmol/l和16.77±0.91μmol/l。这些值随着肾功能的下降而显著增加（P<0.05）。左心室质量指数（LVMI）与两个标志物ADMA（r=0.901，P=0.0001）和iNOS（r=0.718，P=0.0001）之间存在显著正相关。用Vit C和ACEI治疗2年后，观察到LVMI显著下降。
iNOS系统分泌的NO和ADMAs引发心脏重塑，导致左心室肥厚和心脏纤维化。ACEIs增加eNOS的表达和活性并降低iNOS。Vit C通过清除活性氧（ROS）和氮试剂来防止氧化损伤。iNOS和ADMA加速心脏衰老。我们得出结论，ACEIs联合Vit C可能改善CKD患者的心脏健康并限制左心室肥厚。
