Role of an Angiotensin II Type-1 Receptor (AT₁R) Antagonist and Mg²⁺ Supplementation on the Levels of NO_X in Plasma and Kidney Homogenates, Lipid Peroxidation, and Osmotic Fragility of Red Blood Cells in Dahl Rats Fed a High Sodium Diet.

Authors

Lusliany J Rondón, Gabriela González-Infante, Gerardo Moncada, Deliana Rojas, Margrego Piña, Reinaldo Marín

Published in

Biological trace element research. Jul 21, 2026. Epub Jul 21, 2026.

Abstract

Mg²⁺ deficiency has been linked to oxidative stress, inflammation, and hypertension. We have previously shown that Losartan increases plasma Mg²⁺ levels in Dahl salt-sensitive (Dahl) rats, suggesting that defective Mg²⁺ metabolism in this strain contributes to hypertension. Here, we investigated the effects of dietary Mg²⁺ supplementation (0.3% MgO) and/or Losartan (10 mg/kg/day, in drinking water) in male Dahl rats fed a high-NaCl (8%) or standard Na⁺ diet for six weeks. Six-week-old rats were randomly assigned to eight experimental groups. NO metabolites (nitrites and nitrates) were measured in plasma and kidney homogenates. Oxidative stress was assessed by lipid peroxidation in plasma and red blood cell ghosts (RBCG), and by erythrocyte osmotic fragility (OS₅₀). Both Losartan and Mg²⁺ supplementation protected against hypertension and high-salt-induced systemic and local oxidative stress, with differential regulation of Na⁺/K⁺-ATPase and Na⁺-ATPase activity. A consistent "high Na⁺ effect" was observed across NaCl-fed groups, characterized by Renin-Angiotensin-Aldosterone System (RAAS) activation, increased Reactive Oxygen Species (ROS) production, lipid peroxidation, osmotic fragility, and elevated Na⁺/K⁺-ATPase activity. Losartan normalized blood pressure (BP) by attenuating renal RAAS activity and reducing oxidative stress, whereas Mg²⁺ supplementation increased (Nitrites + Nitrates) NO_X levels, improved red blood cell (RBC) membrane stability, and stimulated Na⁺-ATPase activity. These findings highlight distinct but complementary mechanisms through which AT₁R blockade and Mg²⁺ supplementation attenuate salt-induced oxidative stress and reduce BP. Future studies incorporating immunohistochemistry and qPCR are warranted to further characterize ROS-mediated renal tissue damage across treatment groups.

PMID:
42479123
Bibliographic data and abstract were imported from PubMed on 21 Jul 2026.

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