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Although the final TCP was similar in LS and normal sodium rats infused with high and low doses of angiotensin II, respectively, the rise in HWI was blocked by the LS diet. In LS rats, the increased production of O[Formula: see text] and H 2 O 2 was abrogated. The beneficial effects of dietary sodium restriction on target organ damage caused by angiotensin II are independent of arterial pressure rise and may be due to attenuation of the peptide's prooxidant effects.
Source link: https://doi.org/10.1152/ajpheart.00864.2002
Patients with chronic kidney disease have an elevated Fibroblast growth factor 23 that contributes to left ventricular hypertrophy. AngII 70 vs. 196 pmol/L]; Aldosterone 130 vs. 196 pmol/L]: Compared to healthy individuals, the RAAS' PRA-S, AngII, and aldosterone were generally lower [median PRA-S 130 vs. 196 pmol/L]. There was no evidence that the effect of FGF23 on LVH was mediated by RAAS parameters, as shown by all estimated indirect effects virtually zero. No association was found between RAFAS and LVMI change analysis, although there was a strong correlation between FGF23 levels and left ventricular mass index at the end of the study and the FGF23 fold change and LVMI change analysis, no correlation was found between RAAS and LVMI. In healthy controls, serum concentrations of PRA-S, AngII, and aldosterone were below those determined in healthy controls, indicating that RAAS is not systemically activated in hemodialysis patients.
Source link: https://doi.org/10.3389/fmed.2022.878730
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