Dietary sodium loading impairs microvascular function independent of blood pressure in humans: role of oxidative stress
Sodium nitroprusside
Microdialysis
DOI:
10.1113/jphysiol.2012.236992
Publication Date:
2012-08-21T02:07:56Z
AUTHORS (6)
ABSTRACT
Key points Pre‐clinical studies suggest that acute dietary sodium loading impairs vascular function without alterations in blood pressure; however, human data are lacking. In this study, normotensive salt‐resistant adults participated a controlled feeding which they consumed low‐sodium diet for 1 week and high‐sodium week, random order. During each diet, microvascular was assessed. Here we report the novel finding of sodium‐induced impairments independent pressure healthy adults. We additionally show improved by administration anti‐oxidant ascorbic acid. Therefore, addition to its well‐known importance control, lowering intake may have beneficial effects on Abstract Animal reported salt‐induced reductions increases (BP). The purpose study determine if short‐term cutaneous with salt resistance. Following control run‐in 12 (31 ± 2 years) were randomized 7 day (LS; 20 mmol −1 ) (HS; 350 (controlled study). Salt resistance, defined as ≤5 mmHg change 24 h mean BP determined while LS HS diets, confirmed all subjects undergoing (LS: 84 vs. HS: 85 mmHg; P > 0.05). On last instrumented two microdialysis fibres local delivery Ringer solution m acid (AA). Laser Doppler flowmetry used measure red cell flux during heating‐induced vasodilatation (42°C). After established plateau, 10 l ‐NAME perfused quantify NO‐dependent vasodilatation. All expressed percentage maximal conductance (CVC) at site (28 nitroprusside; 43°C). Sodium excretion increased ( < plateau % CVCmax reduced 93 80 CVCmax; AA (Ringer: AA: 89 3 0.05) restored NO contribution 44 59 6 These demonstrate role oxidative stress.
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