Endothelial dysfunction in normotensive salt-sensitive subjects

Fq, Liu; Jj, Mu; Zq, Liu; Dc, Shi; Huang, Qiang; Yuan, Zuyi; Qf, Lian; Sh, Zheng

doi:10.1038/jhh.2011.13

Cited by 18 publications

(20 citation statements)

References 27 publications

(34 reference statements)

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“…5 Our previous dietary intervention studies also showed that a high-salt diet can impair endothelial function and facilitate inflammation in normotensive subjects, especially in salt-sensitive patients. 29, 30 Our present study demonstrated that salt loading significantly enhanced the plasma OPG level and that the 24-h urinary sodium excretion positively associated with the OPG level in humans. This study provided a novel finding that explains the link between sodium intake and CVD incidence.…”

Section: Effects Of High Salt Intake and Potassium Supplementation Onsupporting

confidence: 58%

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

Liu

Zhang

et al. 2017

Circ J

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Osteoprotegerin (OPG), a soluble member of the tumor necrosis factor (TNF) receptor superfamily, acts as a decoy receptor of the receptor activator of nuclear factor κ-B ligand (RANKL) and the TNF-related apoptosis-inducing ligand (TRAIL); RANKL and TRAIL are 2 cytokines of the TNF family mainly involved in bone metabolism; they are also found in other tissues, such as vascular smooth muscle cells. 13 OPG has been implicated in various inflammatory reactions and endothelial dysfunctions, which are also associated with diabetes mellitus and atherosclerosis. 14-16 Increased plasma OPG concentrations are also related to coronary artery disease frequently accompanied by atherosclerosis, stroke, diabetes mellitus, vascular death, and overall cardiovascular morbidity and mortality. [17][18][19][20] Data are still scarce in the literature with regard to the link between salt intake and OPG. Our study was designed to examine the effects of salt intake and potassium supple-E xcess dietary salt induces adverse cardiovascular and renal effects, as demonstrated in numerous epidemiological, interventional, and experimental studies. 1-3 Hypertension prevention studies have provided supporting evidence that modest reductions in salt intake promote 25% long-term reduction in the risk of cardiovascular events; thus, salt intake is implicated in cardiovascular function. 4 Several mechanisms, including endothelial dysfunction, oxidative stress, inflammation, insulin resistance, and neurogenically mediated increase in peripheral resistance, contribute to the harmful effects of dietary salt. 5-9 Potassium likely elicits favorable effects on cardiovascular morbidity and mortality. 10-12 Dietary potassium supplementation may prevent the salt loading-induced elevation of blood pressure (BP) by inhibiting the sympathetic nerve excitability, salt-induced insulin resistance, and oxygen-reactive free radical generation. Background: Excess dietary salt is strongly correlated with cardiovascular disease, morbidity, and mortality. Conversely, potassium likely elicits favorable effects on cardiovascular disorders. In epidemiological studies, increased plasma osteoprotegerin (OPG) concentrations are associated with atherosclerosis and vascular deaths. Our study was designed to examine the effects of salt intake and potassium supplementation on plasma OPG levels in normotensive subjects.

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Section: Effects Of High Salt Intake and Potassium Supplementation Onsupporting

confidence: 58%

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

Liu

Zhang

et al. 2017

Circ J

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“…; Liu et al . ), whereas others failed to demonstrate such a relationship (Stein et al . ; Higashi et al .…”

Section: Introductionmentioning

confidence: 96%

The role of cyclo‐oxygenase‐1 in high‐salt diet‐induced microvascular dysfunction in humans

Čavka

Ćosić

Jukić

et al. 2015

The Journal of Physiology

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Key pointsr Recent studies have shown that some of the deleterious effects of a high-salt (HS) diet are independent of elevated blood pressure and are associated with impaired endothelial function.r Increased generation of cyclo-oxygenase (COX-1 and COX-2)-derived vasoconstrictor factors and endothelial activation may contribute to impaired vascular relaxation during HS loading.r The present study aimed to assess the regulation of microvascular reactivity and to clarify the role of COX-1 and COX-2 in normotensive subjects on a short-term HS diet.r The present study demonstrates the important role of COX-1 derived vasoconstrictor metabolites in regulation of microvascular blood flow during a HS diet.r These results help to explain how even short-term HS diets may impact upon microvascular reactivity without changes in blood pressure and suggest that a vasoconstrictor metabolite of COX-1 could play a role in this impaired tissue blood flow. AbstractThe present study aimed to assess the effect of a 1-week high-salt (HS) diet on the role of cyclo-oxygenases (COX-1 and COX-2) and the vasoconstrictor prostaglandins, thromboxane A 2 (TXA 2 ) and prostaglandin F 2α (PGF 2α ), on skin microcirculatory blood flow, as well as to detect its effect on markers of endothelial activation such as soluble cell adhesion molecules. Young women (n = 54) were assigned to either the HS diet group (N = 30) (ß14 g day -1 NaCl ) or low-salt (LS) diet group (N = 24) (<2.3 g day -1 NaCl ) for 7 days. Post-occlusive reactive hyperaemia (PORH) in the skin microcirculation was assessed by laser Doppler flowmetry. Plasma renin activity, plasma aldosterone, plasma and 24 h urine sodium and potassium, plasma concentrations of TXB 2 (stable TXA 2 metabolite) and PGF 2α , soluble cell adhesion molecules and blood pressure were measured before and after the diet protocols. One HS diet group subset received 100 mg of indomethacin (non-selective COX-1 and COX-2 inhibitor), and another HS group subset received 200 mg of celecoxib (selective COX-2 inhibitor) before repeating laser Doppler flowmetry measurements. Blood pressure was unchanged after the HS diet, although it significantly reduced after the LS diet. Twenty-four hour urinary sodium was increased, and plasma renin activity and plasma aldosterone levels were decreased after the HS diet. The HS diet significantly impaired PORH and increased TXA 2 but did not change PGF 2α levels. Indomethacin restored microcirculatory blood flow and reduced TXA 2 . By contrast, celecoxib decreased TXA 2 levels but had no significant effects on blood flow. Restoration of of PORH by indomethacin during a HS diet suggests an important role of COX-1 derived vasoconstrictor metabolites in the regulation of microvascular blood flow during HS intake.

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“…These results indicated that salt independent of blood pressure significantly affect DDAH (particularly DDAH-2) and eNOS expression, which represented the physiopathological condition of PRMT/ADMA/DDAH pathway dysregulation prior to blood pressure elevation. This could account for our previous finding that endothelial dysfunction already existed in normotensive salt-sensitive subjects [34]. …”

Section: Discussionmentioning

confidence: 61%

Impact of High Salt Independent of Blood Pressure on PRMT/ADMA/DDAH Pathway in the Aorta of Dahl Salt-Sensitive Rats

Cao

Yuan

et al. 2013

IJMS

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Endothelial dysfunction participates in the development and progression of salt-sensitive hypertension. Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthase (NOS). The objectives of this study were to investigate the impact of a high salt diet on the PRMT/ADMA/DDAH (protein arginine methyltransferases; dimethylarginine dimethylaminohydrolase) pathway in Dahl salt-sensitive (DS) rats and SS-13BN consomic (DR) rats, and to explore the mechanisms that regulate ADMA metabolism independent of blood pressure reduction. Plasma levels of nitric oxide (NO) in DS rats given a high salt diet and subjected to intragastric administration of hydralazine (SH + HYD group) were lower than those given a normal salt diet (SN group). There were significant decreases in expression and activity of dimethylarginine dimethylaminohydrolase (DDAH) and endothelial NO synthase (eNOS) in DS rats given a high diet (SH group) in comparison to the SN group. The activity of DDAH and expression of eNOS in the SH + HYD group decreased more significantly than SN group. The mRNA expression of DDAH-1 and DDAH-2 were lowest in the SH group. The results suggest that salt, independent of blood pressure, can affect the PRMT-1/ADMA/DDAH system to a certain degree and lead to endothelial dysfunction in Dahl salt-sensitive rats.

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Endothelial dysfunction in normotensive salt-sensitive subjects

Cited by 18 publications

References 27 publications

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

Effects of Salt Loading on Plasma Osteoprotegerin Levels and Protective Role of Potassium Supplement in Normotensive Subjects

The role of cyclo‐oxygenase‐1 in high‐salt diet‐induced microvascular dysfunction in humans

Impact of High Salt Independent of Blood Pressure on PRMT/ADMA/DDAH Pathway in the Aorta of Dahl Salt-Sensitive Rats

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