Abstract
Despite decades of efforts to reduce sodium intake, excess dietary sodium remains commonplace, and contributes to increased cardiovascular morbidity and mortality independent of its effects on blood pressure. An increasing amount of research suggests that high-sodium diets lead to reduced nitric oxide-mediated endothelial function, even in the absence of a change in blood pressure. As endothelial dysfunction is an early step in the progression of cardiovascular diseases, the endothelium presents a target for interventions aimed at reducing the impact of excess dietary sodium. In this review, we briefly define endothelial function and present the literature demonstrating that excess dietary sodium results in impaired endothelial function. We then discuss the mechanisms through which sodium impairs the endothelium, including increased reactive oxygen species, decreased intrinsic antioxidant defenses, endothelial cell stiffening, and damage to the endothelial glycocalyx. Finally, we present selected research findings suggesting that aerobic exercise or increased intake of dietary potassium may counteract the deleterious vascular effects of a high-sodium diet.
Highlights
Over 90% of adults in the United States consume high-salt diets, with an average daily sodium intake of 3600 mg, which far exceeds the 2300 mg/day as recommended in the Dietary Guidelines for Americans [1,2]
ACh-induced dilation was reduced by HS compared to LS in the control group, but this decrement did not occur in the group that supplemented with vitamin C and E
Raij and colleagues demonstrated that the addition of 3.6% potassium citrate to a high-sodium diet (8% sodium chloride) mitigated sodium-induced endothelial dysfunction in Dahl salt-sensitive rats, independent of any effect on blood pressure (BP), providing support for the use of potassium to combat the vascular consequences of excess dietary sodium [107]
Summary
Over 90% of adults in the United States consume high-salt diets, with an average daily sodium intake of 3600 mg, which far exceeds the 2300 mg/day as recommended in the Dietary Guidelines for Americans [1,2]. Even in the absence of elevated BP, high dietary sodium is associated with negative impacts on cardiovascular health. Overweight individuals in the highest quartile of sodium intake have an increased risk of congestive heart failure compared to those in the lowest quartile, even after controlling for demographics, alcohol consumption, smoking, physical activity, and BP [11]. Overweight individuals in the highest quartile of sodium intake have an increased risk of congestive heart failure compared to those in the lowest quartile, 2eovfe1n7 after controlling for demographics, alcohol consumption, smoking, physical activity, and BP [11]. Greater sodium intake is related to greater left ventricular mass in both normotensive and hypertensive individuals [12,13], and left ventricular hypertrophy iasnrdevheyrpseedrtewnisthivseoidniduimvidreudaulsct[i1o2n,1[31]4, ]a.nNdolteafbtlvye, nentrdicouthlaerlihayl pdeyrstfruonpchtiyonisorfetveenrpserdecweditehs tmeespAsoeerbhuifxoffhfezdfffaecmdeceeeemrdeaccincskdmsuittrtAAoitessstsdemtihamriosvsoiogsoreonoefooofreiafvzlflaehunudetoiaeldtethitxotilpsghesllduyuicnciirmhge,nnemuca.tbrhsteeddhteleiysAauddnoieecimdrervlepntdiiteeidnnnelaahdetoi[ierteytt1FydsiFfyaxetrre4isiiiriraegbeagcos]ioaympc.oatuseunutaaeNordurraissrldmrenei(rolyoutaCeliei1sd1yotincfmstVa,,f,ivtsoigeetubitguDahdvcrxhclmtasgeoytiiaih)itscstusc,gnme[eyuere1meocsrdenlpnei5suoofanvtvt–odnrmcerbii1titoonxseiyrehep7dnunecwtgwna]htepcimspitstaresuopoipthetensalphnmrhrairyialdatteveeseosssimplsseoeetinveedtchpndseidnnaa(euyuoocCislttndsnsohgtessceVfdaitn.gaumutetnacohnDheltnrttaateaseieiyih)csyratvnrctmecylsidc[ibutultoo1ohiysoeprmra5ndnartrrloa–hieseoteeoufn1tennecusraf7mtqhlptttenshi]eiuaeaasoecnencirvenlavntucloininiipyvsorfdmdsncieudranmbmeseeaensunlnsiccsctseancoceemhcuotrfeeddnhiukrfloopaeefusefsernortosdusrmxitprrmoimtcohcieoahBnBenfoitanpnsesP.aPtnysshtsrh-p-dsi,iiyiesoeubhnnbeaoqndmlvnededpdeu.needeeoialaelAopupeftonsnnmoaemetuspsecsrnn,mmeesresddmiunisaatomueeehrocnaunnnmolhinadyysstttf-,. Rweveiwewillopfrhoovwidtehaesberibeefhreavviieowrs omfahyowadtdhreesses bspehecaivfiicorms emchayanaidsmdrseossf sdpieetcaifriyc smodeciuhman-iisnmdus coefddeientdaroythseoldiailudmy-sifnudnuccteiodne. ndothelial dysfunction
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