Endothelial function is impaired after a high-salt meal in healthy subjects

Dickinson, Kacie; Clifton, Peter M.; Keogh, Jennifer B.

doi:10.3945/ajcn.110.006155

Cited by 104 publications

(96 citation statements)

References 32 publications

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“…Healthy subjects who received a high-salt meal showed impaired endotheliumdependent vasodilation without any blood pressure changes, possibly because of reduced endothelial nitric oxide synthase activity from increased plasma sodium concentrations. 27 Salt intake has also been associated with inflammatory response; brain and serum levels of an inflammatory marker expressed by endothelial cells, E-selectin, are significantly increased in SHR-SPs after salt intake but unchanged in SHRs. 28 Hence, as demonstrated in the effects of salt and hypertension on endothelial dysfunction, VRFs may directly and indirectly cause endothelial dysfunction, and subsequent BBB breakdown can lead to enlarged perivascular spaces, cerebral microbleeds, and WM changes.…”

Section: Pathogenesis Of Cerebral Small Vessel Disease 555mentioning

confidence: 99%

“…В нескольких других исследованиях по изучению вли-яния пищевой соли на организм человека показали не только ее косвенное (гипертензионно-опосредованное), но и прямое воздействие на эндотелий. У здоровых лиц, получавших большое количество соли, выявили наруше-ние эндотелий-зависимой вазодилатации без каких-либо изменений уровня артериального давления, возможно, из-за снижения активности эндотелиальной синтазы оксида азота в связи с повышением концентрации натрия в плазме крови [27]. Потребление соли также было ассо-циировано с воспалительной реакцией; у КСГПИ после употребления соли отметили значительное повышение содержания Е-селектина, воспалительного маркера, экс-прессируемого эндотелием, в головном мозге и сыворот-ке крови; однако у КСГ таких изменений не было [28].…”

Section: патологический каскад бмцс: роль артериальной гипертензии и unclassified

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Emerging Evidence for Pathogenesis of Sporadic Cerebral Small Vessel Disease

Ihara

Yamamoto

2016

Stroke

127

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Section: Pathogenesis Of Cerebral Small Vessel Disease 555mentioning

confidence: 99%

Section: патологический каскад бмцс: роль артериальной гипертензии и unclassified

Emerging Evidence for Pathogenesis of Sporadic Cerebral Small Vessel Disease

Ihara

Yamamoto

2016

Stroke

127

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“…March 11, 2014 of overall coronary vasodilator capacity and microvascular function. 36 High sodium intake has been positively associated with endothelial dysfunction, 37,38 resistance to the protective effects of renin-angiotensin-aldosterone system blockade (independent of blood pressure), 39,40 and increased left ventricular mass. 41 Conversely, sodium reduction has been shown to decrease left ventricular mass, 42 to improve pulse wave velocity, 43 and to reduce albuminuria in normotensive 44 and hypertensive subjects, 45 independent of blood pressure.…”

Section: Figurementioning

confidence: 99%

Sodium Excretion and Risk of Developing Coronary Heart Disease

et al. 2014

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Background— Despite compelling evidence for sodium’s adverse effects on blood pressure, it remains uncertain whether excess sodium intake is a risk factor for coronary heart disease (CHD) in the overall population and in potentially more susceptible subgroups. Methods and Results— We prospectively followed 7543 adults aged 28 to 75 years and free of cardiovascular and kidney disease in 1997/1998 of the Prevention of Renal and Vascular End-stage Disease (PREVEND) study. Sodium excretion was measured in two 24-hour urine collections at baseline. Potential susceptibility factors were blood pressure and plasma N-terminal pro-B-type natriuretic peptide (NT-proBNP). Median 24-hour sodium excretion was 137 mmol (Q1–Q3, 106–171 mmol). During a median follow-up of 10.5 (Q1–Q3: 9.9–10.8) years, 452 CHD events occurred. In the entire cohort, there was no association between each 1-g/d (43 mmol/24 h) increment in sodium excretion and CHD risk (adjusted hazard ratio, 1.07; 95% confidence interval, 0.98–1.18; P =0.15). However, the association of sodium excretion with CHD risk tended to be modified by mean arterial pressure ( P interaction =0.08) and was modified by NT-proBNP ( P interaction =0.002). When stratified, each 1-g/d increment in sodium excretion was associated with an increased risk for CHD in subjects with hypertension (adjusted hazard ratio, 1.14; 95% confidence interval, 1.01–1.28; n=2363) and in subjects with NT-proBNP concentrations above the sex-specific median (adjusted hazard ratio, 1.16; 95% confidence interval, 1.03–1.30; n=3771). Conclusions— Overall, there was no association between sodium excretion and risk of CHD. The association between sodium excretion and CHD risk was modified by NT-proBNP. Higher sodium excretion was associated with an increased CHD risk among subjects with increased NT-proBNP concentrations or with hypertension.

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“…46) Regarding vascular damage, it has been shown that high dietary salt decreases plasma nitrate and nitrite and impairs endothelial function in humans. 47,48) The salt-induced endothelial dysfunction and damage may promote structural changes in arteries and kidney disease. 49) High sodium intake has been associated with increased carotid intima-media thickness in obese subjects, and with central pulse pressure and augmentation index in hypertensive patients.…”

Section: Salt and Organ Damagementioning

confidence: 99%

Salt, Hypertension, and Cardiovascular Diseases

Kawano

2012

J Korean Soc Hypertens

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❙ABSTRACT❙The relationship between salt and hypertension is well established, and salt restriction is widely recommended in the management of hypertension. However, people living in northeast Asia have consumed large amount of salt, and the prevalence of hypertension and the incidence of stroke have been high in that area. Mechanisms of salt-induced hypertension may be complex, but volume expansion in the presence of impaired natriuretic capacity of the kidney and action on the central nervous system and neurohormoral pathways seem to be important. Salt is also involved in changes in blood pressure (BP) caused by other factors, such as weight gain, stress, exercise, potassium, catecholamines, angiotensin, and aldosterone. The interaction between sodium and aldosterone appears to play a critical role in the development of organ damage. The depressor effect of salt restriction in hypertensive patients is well demonstrated although the response of BP varies widely among individuals. Salt restriction decreases BP throughout 24 hours, and its effect may be greater during night compared to daytime in salt-sensitive nondippers. Although excess salt consumption can cause cardiovascular diseases through its effect on BP, recent studied have shown that the association of salt consumption and cardiovascular diseases, such as stroke and heart failure, is independent of BP. Salt reduction is important in the prevention of cardiovascular diseases, however, the effect and safety of aggressive salt restriction remain to be clarified. It is difficult to accomplish and maintain the salt reduction. Both population strategy and individualized approach are important to reduce salt consumption.

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Endothelial function is impaired after a high-salt meal in healthy subjects

Cited by 104 publications

References 32 publications

Emerging Evidence for Pathogenesis of Sporadic Cerebral Small Vessel Disease

Emerging Evidence for Pathogenesis of Sporadic Cerebral Small Vessel Disease

Sodium Excretion and Risk of Developing Coronary Heart Disease

Salt, Hypertension, and Cardiovascular Diseases

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