Angiotensin II Exposure In Vitro Reduces High Salt-Induced Reactive Oxygen Species Production and Modulates Cell Adhesion Molecules’ Expression in Human Aortic Endothelial Cell Line

Abstract

Background/Objectives: Increased sodium chloride (NaCl) intake led to leukocyte activation and impaired vasodilatation via increased oxidative stress in human/animal models. Interestingly, subpressor doses of angiotensin II (AngII) restored endothelium-dependent vascular reactivity, which was impaired in a high-salt (HS) diet in animal models. Therefore, the present study aimed to assess the effects of AngII exposure following high salt (HS) loading on endothelial cells’ (ECs’) viability, activation, and reactive oxygen species (ROS) production. Methods: The fifth passage of human aortic endothelial cells (HAECs) was cultured for 24, 48, and 72 h with NaCl, namely, the control (270 mOsmol/kg), HS320 (320 mOsmol/kg), and HS350 (350 mOsmol/kg). AngII was administered at the half-time of the NaCl incubation (10−4–10−7 mol/L). Results: The cell viability was significantly reduced after 24 h in the HS350 group and in all groups after longer incubation. AngII partly preserved the viability in the HAECs with shorter exposure and lower concentrations of NaCl. Intracellular hydrogen peroxide (H2O2) and peroxynitrite (ONOO−) significantly increased in the HS320 group following AngII exposure compared to the control, while it decreased in the HS350 group compared to the HS control. A significant decrease in superoxide anion (O2.−) formation was observed following AngII exposure at 10−5, 10−6, and 10−7 mol/L for both HS groups. There was a significant decrease in intracellular adhesion molecule 1 (ICAM-1) and endoglin expression in both groups following treatment with 10−4 and 10−5 mol/L of AngII. Conclusions: The results demonstrated that AngII significantly reduced ROS production at HS350 concentrations and modulated the viability, proliferation, and activation states in ECs.