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Low sodium intake is paradoxically associated with adverse cardiovascular outcomes in individuals with type 2 diabetes (T2D), possibly from renin-angiotensin-aldosterone system (RAAS) activation, leading to endothelial dysfunction. In this study, we investigated the associations between habitual sodium intake and RAAS blockade on endothelial function by measuring circulating microparticles (MPs) in individuals with T2D. We conducted a prospective, cross-sectional studyin 74 individuals with T2D. Habitual dietary sodium intake was estimated using the mean of three corrected 24-hour urine sodium excretion measurements (24hUNa). MP subtypes in platelet-free plasma were quantified using flow cytometry.No associations between 24hUNa with levels of endothelial MPs were observed. Instead, a trend towards higher diabetes related CD36+/CD235a+ MP levels was associated with lower 24hUNa (rho = -0.23, p= 0.05). When stratified according to tertiles of 24hUNa, platelet- derived CD42b+/CD41+ and CD42+/CD41+/Annexin V+ MPs were higher in the lowest tertile (24hUNa <157mmol/24h) (p=0.02 respectively). Despite RAAS blockade being associated with lower levels of most MP subsets, it was not associated with lower MPs, in the setting of low sodium intake. In conclusion, lower sodium intake is associated with higher circulating procoagulant MPs but not with evidence of endothelial dysfunction in individuals with T2D. |
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