Short-term high salt intake reduces brachial artery and microvascular function in the absence of changes in blood pressure

Čavka, Ana; Jukić, Ivana; Ali, Mohamed M.; Goslawski, Melissa; Bian, Jing; Wang, Edward; Drenjančević-Perić, Ines; Phillips, Shane A.

doi:10.1097/hjh.0000000000000852

Cited by 32 publications

(45 citation statements)

References 51 publications

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“…These studies are summarized in Table . The outcomes examined were diverse: one study assessed mortality outcomes (category I), two studies assessed morbidity outcomes (category II), two studies assessed outcomes related to symptoms/quality of life/functional status (category III), six studies assessed BP outcomes (category IV), seven studies assessed other clinically relevant surrogate outcomes (category V), and 10 studies assessed physiologic outcomes (category VI) …”

Section: Resultsmentioning

confidence: 99%

“…No primary research studies in the physiologic category (category VI) met the minimum methodological criteria. A range of outcomes were captured by the studies considered to be of lower quality, including all‐cause mortality, headaches/migranes, BP, cognitive function, acne, obesity and ghrelin, multiple sclerosis, BMD, gastric cancer, flow‐mediated dilatation, pulse wave velocity, markers of the renin‐angiotensin‐aldosterone system, heart rate, insulin resistance and the metabolic syndrome, brain tissue white matter hyperintensity, uric acid, and urinary albumin . Most of these studies found adverse effects of dietary salt on health, except for three that were neutral and one that found an inverse relationship between salt intake and headaches/migranes …”

Section: Resultsmentioning

confidence: 99%

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More evidence that salt increases blood pressure and risk of kidney disease from the Science of Salt: A regularly updated systematic review of salt and health outcomes (April–July 2016)

Arcand

Wong

Santos

et al. 2017

J of Clinical Hypertension

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The purpose of this review is to identify, summarize, and critically appraise studies on dietary salt and health outcomes that were published from April to July 2016. The search strategy was adapted from a previous systematic review on dietary salt and health. We have revised our criteria for methodological quality and health outcomes, which are applied to select studies for detailed critical appraisals and written commentary. Overall, 28 studies were identified and are summarized in this review. Four of the 28 studies met criteria for methodological quality and health outcomes and five studies underwent detailed critical appraisals and commentary. Three of these studies found adverse effects of salt on health outcomes (chronic kidney disease and blood pressure) and two were neutral (fracture risk/bone mineral density and cognitive impairment). | INTRODUCTIONMeta-analyses and systematic reviews examining the relationship between dietary salt and health outcomes 1,2 have been the basis for consensus that excess salt (sodium) consumption is associated with multiple adverse health outcomes, including a positive causal relationship with blood pressure (BP). The high profile of dietary salt research has resulted in a rapidly growing literature on the health effects of dietary salt. To keep scientific, clinical, and policy stakeholders up to date with the growing body of literature, regularly updated reviews and critical appraisals of studies relating to health outcomes are published in the Journal, alternating with reviews of studies relating to salt reduction implementation programs. 6 The objective of this fourth health outcomes review is to summarize published articles on salt and health outcomes and to highlight and critically appraise the highest-quality articles that were published between April and July 2016. This article also reports on anupdated methodology developed and adopted to ensure an objective review of the most clinically relevant studies. | METHODOLOGYA detailed description of the methodological approach used to identify published articles for this review has been previously reported. 6Briefly, articles were identified on a weekly basis through a MEDLINE search strategy, which was adapted from a previous systematic review used to develop the WHO guideline on dietary sodium intake. 1,2 Figure). Among identified articles, studies were selected to undergo a detailed critical appraisal based on the outcomes examined and methodological quality, as described below. A secondary set of articles was considered for inclusion if judged by the authors to be impactful based on novelty of findings or potential for generating public discourse or scientific controversy or for informing public health policy.Articles were selected for detailed critical appraisal considering a hierarchy of health outcomes, which were those classified based on relevance to patients ( outcome and category I to V outcomes as secondary outcomes, the study was considered for inclusion as long as it met methodological quality criteria.Met...

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

More evidence that salt increases blood pressure and risk of kidney disease from the Science of Salt: A regularly updated systematic review of salt and health outcomes (April–July 2016)

Arcand

Wong

Santos

et al. 2017

J of Clinical Hypertension

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“…Intravenous sodium loading may cause an acute increase in microvascular permeability in healthy male subjects, attributable to adverse effects on the endothelial surface layer . Even short‐term salt intake reduces brachial artery endothelial function and switches the mediator of vasodilation in the microcirculation to a non–nitric‐oxide dependent mechanism, even in healthy adults …”

Section: Microvascular Dysfunction Associated With High‐salt Intake Imentioning

confidence: 99%

“…31 Even short-term salt intake reduces brachial artery endothelial function and switches the mediator of vasodilation in the microcirculation to a non-nitric-oxide dependent mechanism, even in healthy adults. 32 Also the activity of the renin angiotensin system can be modified, since high-salt intake upregulates prorenin-receptor expression in the nephron, which seems to be involved in the regulation of renal dysfunction and proteinuria. 17 A high-salt intake has a negative influence on the homeostatic regulation of vascular bed in hypertensive patients, to a large degree via mechanisms that activate the local renin-angiotensin-aldosterone system in the vessels, 19 or via pathways that inhibit NO production.…”

Section: Crova Scul Ar Dys Fun C Ti On a Sso Ciated With Hi G H mentioning

confidence: 99%

Salt‐induced effects on microvascular function: A critical factor in hypertension mediated organ damage

Marketou

Maragkoudakis

Anastasiou

et al. 2019

J of Clinical Hypertension

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Salt has been linked very closely to the occurrence and complications of arterial hypertension. A large percentage of patients with essential hypertension are salt‐sensitive; that is, their blood pressure increases with increased salt intake and decreases with its reduction. For this reason, emphasis is placed on reducing salt intake to better regulate blood pressure. In day‐to‐day clinical practice this is viewed as mandatory for hypertensive patients who are judged to be salt‐sensitive. Previous studies have highlighted the negative effect of high‐salt diets on macrovascular function, which also affects blood pressure levels by increasing peripheral resistances. More recent studies provide a better overview of the pathophysiology of microvascular disorders and show that they are largely due to the overconsumption of salt. Microvascular lesions, which have a major impact on the functioning of vital organs, are often not well recognized in clinical practice and are not paid sufficient attention. In general, the damage caused by hypertension to the microvascular network is likely to be overlooked, while reversion of the damage is only rarely considered as a therapeutic target by the treating physician. The purpose of this review is to summarize the impact and the harmful consequences of increased salt consumption in the microvascular network, their significance and pathophysiology, and at the same time to place some emphasis on their treatment and reversion, mainly through diet.

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“…Такой резуль тат может показаться неожиданным, но только на первый взгляд. Феномены сольчувствительности и сольрезистентности давно описаны у разных био логических видов -людей, шимпанзе и крыс [6,7]. При этом сольчувствительность (нарастание АД в ответ на повышение потребления хлорида натрия) и сольрезистентность могут встречаться как у нор мотоников, так и гипертоников.…”

Section: результаты исследования и их обсуждениеunclassified

High salts intake, cardiovascular system and kidney in spontaneous hypertensive rats

Кучер

Beresneva

Parastaeva

et al. 2017

Regional blood circulation and microcirculation

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Objective. To study the influence of diet containing high or normal NaCl on the arterial blood pressure level (BP), heart rate (HR), processes of myocardial remodeling and of nuclear transcription factor kB (NFkB) expression in myocardium and kidney in spontaneously hypertensive rats (SHR). Design and methods. The two groups of male SHRs received a diet with normal (0.34 %; n = 24, control) and high content of NaCl (8.0 %; n = 25; experimental group) for 2 months. Blood pressure (BP), heart rate (HR), cardiac left ventricular mass index (LVMI), left (LKMI) and right (RKMI) kidney mass indexes were determined. Morphological study of myocardium (light microscopy), including quantitative morphometry was carried out. In part of animals the relative level of NFkB gene expression in heart and kidney tissues was studied. Results and discussion. In rats fed a diet containing 8 % NaCl BP and HR did not change significantly compared with the control. However, LVMI, RKMI, LKMI were significantly higher in high-salt diet-treated animals than in controls. The heart of high-salt diet-treated animals developed the changes leading to hypertrophy and possibly hyperplasia of cardiomyocytes. In these animals, perivascular fibrosis, significant increase of arterial wall thickness and vacuolization of smooth muscle cells were revealed. The relative level of NFKB gene expression in rats receiving high-salt diet was 33-fold higher in myocardium and 12-fold higher in kidneys than in animals fed a normal salt diet. Conclusion. The high-salt diet is not necessarily accompanied by an increase in blood pressure, but causes myocardial remodeling, apparently due to direct «toxic» effects. The negative impact on the cardiovascular system of high-salt diet is in part mediated through NFkB-associated signaling pathways. Furthermore, high NaCl diet causes activation of NFkB in the kidneys.

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Short-term high salt intake reduces brachial artery and microvascular function in the absence of changes in blood pressure

Cited by 32 publications

References 51 publications

More evidence that salt increases blood pressure and risk of kidney disease from the Science of Salt: A regularly updated systematic review of salt and health outcomes (April–July 2016)

More evidence that salt increases blood pressure and risk of kidney disease from the Science of Salt: A regularly updated systematic review of salt and health outcomes (April–July 2016)

Salt‐induced effects on microvascular function: A critical factor in hypertension mediated organ damage

High salts intake, cardiovascular system and kidney in spontaneous hypertensive rats

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