posted on 2024-06-06, 08:47authored byKozina N., Jukić I., Mihaljević Z., Matić A., DobrivojevićRadmilović M., Barić A., Drenjančević I.
Introduction: High salt (HS) diet increases systemic and vascular oxidative stress in various animal models and in humans, leading to impairment of vascular reactivity. The present study examined the interaction of genotype and HS diet intake and the potential effects of oxidative stress on the flow-induced dilation (FID) in pressurized carotid arteries of normotensive Tff3-/-/C57BL/6N knockout mice and their wild type (WT) controls.
Methods: Male, ten-weeks-old transgenic Tff3−/−/C57BL/6N (Tff3−/−) and WT/C57BL/6N (WT) healthy mice were divided in LS (0.4% NaCl in rodent chow) and HS (4% fed for 1 week) groups.
Results: FID was decreased in WT_HS mice and restored by superoxide scavenger TEMPOL in vivo. Vascular superoxide/ROS levels were increased with HS diet in both strains and restored by TEMPOL. HS upregulated glutathione-peroxidase 1 (GPx1) gene expression in WT_HS and Tff3-/-_ HS mice, while GPx activity was significantly decreased only in WT_ HS group. Serum markers of oxidative stress (oxLDL and AOPP) and arterial blood pressure were similar among groups.
Conclusion: HS diet increases vascular oxidative stress and impairs vasodilation in WT mice. Tff3 gene defficiency attenuates vasodilation per se, without further effects of HS intake.