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Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans.
Ramick, MG, Brian, MS, Matthews, EL, Patik, JC, Seals, DR, Lennon, SL, Farquhar, WB, Edwards, DG
American journal of physiology. Heart and circulatory physiology. 2019;(1):H97-H103
Abstract
It has previously been shown that high dietary salt impairs vascular function independent of changes in blood pressure. Rodent studies suggest that NADPH-derived reactive oxygen species mediate the deleterious effect of high salt on the vasculature, and here we translate these findings to humans. Twenty-nine healthy adults (34 ± 2 yr) participated in a controlled feeding study. Participants completed 7 days of a low-sodium diet (LS; 20 mmol sodium/day) and 7 days of a high-sodium diet (HS; 300 mmol sodium/day) in random order. All participants were salt resistant, defined as a ≤5-mmHg change in 24-h mean BP determined while on the LS and HS diets. Laser Doppler flowmetry was used to assess cutaneous vasodilation in response to local heating (42°C) during local delivery of Ringer's (n = 29), 20 mM ascorbic acid (AA; n = 29), 10 µM Tempol (n = 22), and 100 µM apocynin (n = 22). Additionally, endothelial cells were obtained in a subset of participants from an antecubital vein and stained for nitrotyrosine (n = 14). Cutaneous vasodilation was attenuated by the HS diet compared with LS [LS 93.0 ± 2.2 vs. HS 86.8 ± 2.0 percentage of maximal cutaneous vascular conductance (%CVCmax); P < 0.05] and was restored by AA during the HS diet (AA 90.7 ± 1.2 %CVCmax; P < 0.05 vs. HS). Cutaneous vasodilation was also restored with the local infusion of both apocynin (P < 0.01) and Tempol (P < 0.05) on the HS diet. Nitrotyrosine expression was increased on the HS diet compared with LS (P < 0.05). These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. NEW & NOTEWORTHY High-sodium diets have deleterious effects on vascular function, likely mediating, in part, the increased cardiovascular risk associated with a high sodium intake. Local infusion of apocynin and Tempol improved microvascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt. This study provides insight into the blood pressure-independent mechanisms by which dietary sodium impairs vascular function. Listen to this article's corresponding podcast at https://ajpheart.podbean.com/e/dietary-sodium-oxidative-stress-and-microvascular-function/ .
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[New aspects of the pathomechanism of salt-sensitive hypertension].
Sulyok, E
Orvosi hetilap. 2019;(2):43-49
Abstract
This article shortly outlines the evolution of hypertonia from risk factors to end-organ damage. The pathogenetic role of salt intake is underlined and in the light of recent clinical and experimental observations, the importance of renal and extrarenal mechanism in the development of salt-sensitive hypertension is analysed. The generally accepted concept that the inefficient renal sodium excretion and the subsequent expansion of the extracellular space is the major factor in blood pressure elevation is challenged. Evidences have been provided that the retained sodium dissociates from the volume of extracellular space and, also from the blood pressure. It has been shown that the negatively charged macromolecules in the subcutaneous interstitium bind sodium ions in osmotically inactive form and store sodium reversibly. The local tissue hypertonicity induces monocytes/macrophages invasion and activation that causes increased expression of tonicity-responsive enhancer binding protein (TonEBP) and the secretion of vascular endothelial growth factor C that result in enhanced lymphangiogenesis. The expanded lymphatic system drains the excess sodium and volume back to the circulation. The reduction of buffer function of this system may contribute to the development or to worsening of hypertension. Similar buffer and barrier functions are attributed to the glycocalyx that covers the luminal surface of vascular endothelium. It is also recognised that the high sodium intake alone is an important pathogenetic factor in end-organ damage independent of hypertension. This may be accounted for by the induction and activation of Th17 cells as well as by the increased production of several pro-inflammatory and pro-fibrotic cytokines. Orv Hetil. 2019; 160(2): 43-49.
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The effect of dietary salt on blood pressure in individuals receiving chronic dialysis: a systematic review and meta-analysis of randomised controlled trials.
Cole, NI, Swift, PA, He, FJ, MacGregor, GA, Suckling, RJ
Journal of human hypertension. 2019;(4):319-326
Abstract
Dietary salt reduction in the general population lowers blood pressure and cardiovascular risk. Despite being widely recommended, there is limited evidence as to whether this is applicable to individuals with end-stage renal disease (ESRD) receiving dialysis. Therefore, we carried out a systematic review and meta-analysis of randomised controlled trials (RCTs) investigating dietary salt reduction in individuals receiving dialysis. Studies were identified through search strategies for CENTRAL, MEDLINE, and EMBASE. Two authors independently assessed studies for eligibility with the inclusion criteria as follows: participants aged 18 years and over; a reduction in salt intake of at least 1 g/day over one week; no concomitant interventions during the study. The primary outcome was change in systolic and diastolic blood pressure. 848 reports were screened, from which 12 studies were selected for the systematic review. Four were RCTs (91 participants) that met the study inclusion criteria: three were conducted in haemodialysis patients and one in peritoneal dialysis patients; three were crossover trials and one was a parallel study. Dietary salt reduction was associated with an 8.4 mmHg reduction in systolic blood pressure (95% CI 4.8-12.0, Ι2 = 0%), and a 4.4 mmHg reduction in diastolic blood pressure (95% CI 2.2-6.6, Ι2 = 0%). In conclusion, few studies have investigated the role of dietary salt reduction in individuals with ESRD receiving dialysis, but these results suggest the importance of this intervention for lowering blood pressure in this group.
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High-salt intake affects sublingual microcirculation and is linked to body weight change in healthy volunteers: a randomized cross-over trial.
Rorije, NMG, Rademaker, E, Schrooten, EM, Wouda, RD, Homan Van Der Heide, JJ, Van Den Born, BH, Vogt, L
Journal of hypertension. 2019;(6):1254-1261
Abstract
BACKGROUND The pathophysiology of salt-sensitive hypertension remains uncertain, but may involve microvascular alterations. High-salt intake decreases microvascular density in hypertensive patients, but due to lack of studies in normotensive patients the causal pathway remains unclear. We studied whether high-salt intake decreases sublingual microvascular density in normotensive individuals and assessed the influence of body weight on changes in microvascular density. METHODS In an open label randomized cross-over trial 18 healthy men were included to study the effect of a 2-week high-salt (>12 g/day) and low-salt (<3 g/day) diet on microvascular (diameter <20 μm) density with sublingual sidestream darkfield imaging. We used sublingual nitroglycerin (NTG) to recruit microvessels. RESULTS There was no significant difference in microvascular density between diets (0.96 ± 3.88 mm/mm; P = 0.31, following NTG; and -0.03 ± 1.64 mm/mm; P = 0.95, without NTG). Increased salt intake was correlated with a decrease in microvascular density following NTG (r = -0.47; P = 0.047), but not without NTG (r = 0.06; P = 0.800). The decrease in microvascular density following high-salt intake was significantly larger for those with a large change in body weight as compared with those with a small changer in body weight (-0.79 ± 1.35 and 0.84 ± 1.56 mm/mm respectively, P = 0.031). CONCLUSION We demonstrate in healthy volunteers that higher salt intake is correlated with decreased sublingual microvascular density following administration of NTG and; larger changes in body weight following high-salt intake coincide with a larger decrease in microvascular density. Changes in microvascular density occurred without blood pressure effects, indicating that high-salt load as such contributes to microvascular changes, and may precede hypertension development.
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Dose-response relation between dietary sodium and blood pressure: a meta-regression analysis of 133 randomized controlled trials.
Graudal, N, Hubeck-Graudal, T, Jürgens, G, Taylor, RS
The American journal of clinical nutrition. 2019;(5):1273-1278
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Abstract
BACKGROUND The projected reduced mortality effect of reduced sodium intake in model-based studies conflicts with the observed increased mortality associated with low sodium intake in population studies. This may reflect an overestimation of the dose-response relation between sodium reduction (SR) and blood pressure (BP) used in mortality modeling studies. OBJECTIVES The present meta-regression analysis sought to estimate the dose-response relations between SR and BP in study groups with mean BP above or below the 75th percentile of the general population. METHODS Based on a literature search from 1 January 1946 to 11 April 2018, we identified 133 randomized controlled trials allocating healthy or hypertensive individuals to SR or usual sodium intake. Multivariable regression analyses of the mean SR versus the mean blood pressure effect adjusted for effect modifiers were performed. RESULTS In study groups with mean BP above the 75th percentile [131/78 mm Hg systolic BP (SBP)/diastolic BP (DBP)], there was strong evidence of a linear dose-response relation between SR and BP. For SBP, the dose-response relation was -7.7 mm Hg/100 mmol SR (95% CI: -10.4, -5.0), and for DBP it was -3.0 mm Hg/100 mmol SR (95% CI: -4.6, -1.4). In study groups with mean BP ≤ 131/78 mm Hg, the relation between SR and BP was weak. For SBP it was -1.46 mm Hg/100 mmol SR (95% CI: -2.7, -0.20) and for DBP it was: -0.07 mm Hg/100 mmol SR (95% CI: -1.5, 1.4). CONCLUSIONS Only study groups with a BP in the highest 25th percentile of the population showed a clinically significant drop in BP with SR. The policy of lowering dietary sodium intake in the general population may need to be reframed to target patients with hypertension. This study was registered at PROSPERO 2015 as CRD42015017773.
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[Salt sensitivity and hypertension].
Chatelanat, O, Pechère-Bertschi, A, Ponte, B
Revue medicale suisse. 2019;(662):1625-1628
Abstract
The salt sensitivity of the blood pressure (SSBP) is defined as a rise or fall in blood pressure induced by a change in sodium intake. There is an interindividual variation and no strong diagnostic criteria exist to date. The SSBP may lead to underestimation of the beneficial effect of sodium restriction in some patients in meta-analyzes. High sodium intake in salt sensitive patients results in an increase in the prevalence of hypertension and target organ damage. The etiology seems to be a failure of one or more natriuretic mechanisms. Some environmental, genetic and epidemiological factors increase its susceptibility. Per se, SSBP cannot be treated, but its identification may help in preventing hypertension and adapt the treatment in some populations.
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The Impact of Herbs and Spices on Increasing the Appreciation and Intake of Low-Salt Legume-Based Meals.
Dougkas, A, Vannereux, M, Giboreau, A
Nutrients. 2019;(12)
Abstract
Flavoring using blends of herbs and spices (H&S) instead of salt may be a promising approach to increase legume consumption and reduce salt content in foods. This study examines the effects of H&S on the appreciation and intake of low-salt legume-based dishes in a real ecological eating environment. Four mezzes with standard (0.8% w/w) (S) or lower (0.4% w/w) (LS) salt level and with or without H&S (LSHS, SHS) were developed. In a randomized cross-over trial, 94 participants attended four sessions, one week apart and received the four variants as a starter during lunch. Overall liking, food intake, and appetite ratings (visual analogue scale, VAS) were assessed during lunch. A follow-up study (n = 130) was performed where the four variants were evaluated, and overall liking was measured at the same session. Overall liking and taste scores of SHS were significantly higher compared with LS (p = 0.04 and p = 0.03, respectively), but there were no significant differences between LSHS and S. However, there were no differences in energy intake or in appetite ratings among the products. Overall appreciation was similar between the low-salt with H&S and the standard-salt mezze, suggesting that the addition of H&S is a feasible strategy for achieving a 50% reduction in salt content without compromising hedonic appreciation.
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Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow.
Babcock, MC, Robinson, AT, Migdal, KU, Watso, JC, Wenner, MM, Stocker, SD, Farquhar, WB
Hypertension (Dallas, Tex. : 1979). 2019;(3):587-593
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Abstract
The American Heart Association recommends no more than 1500 mg of sodium/day as ideal. Some cohort studies suggest low-sodium intake is associated with increased cardiovascular mortality. Extremely low-sodium diets (≤500 mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow. The effects of an American Heart Association-recommended diet on sympathetic regulation of the vasculature are unclear. Therefore, we assessed whether a 1000 mg/d diet alters sympathetic outflow and sympathetic vascular transduction compared with the more commonly recommended 2300 mg/d. We hypothesized that sodium reduction from 2300 to 1000 mg/d would not affect resting sympathetic outflow but would reduce sympathetic transduction in healthy young adults. Seventeen participants (age: 26±2 years, 9F/8M) completed 10-day 2300 and 1000 mg/d sodium diets in this randomized controlled feeding study (crossover). We measured resting renin activity, angiotensin II, aldosterone, blood pressure, muscle sympathetic nerve activity, and norepinephrine. We quantified beat-by-beat changes in mean arterial pressure and leg vascular conductance (femoral artery ultrasound) following spontaneous sympathetic bursts to assess sympathetic vascular transduction. Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P<0.01 for all) but did not alter mean arterial pressure (78±2 versus 77±2 mm Hg, P=0.56), muscle sympathetic nerve activity (13.9±1.3 versus 13.9±0.8 bursts/min, P=0.98), or plasma/urine norepinephrine. Sympathetic vascular transduction decreased ( P<0.01). These data suggest that reducing sodium from 2300 to 1000 mg/d stimulates the renin-angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults.
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Evaluation of an education program based on the theory of planned behavior for salt intake in individuals at risk of hypertension.
Rahimdel, T, Morowatisharifabad, MA, Salehi-Abargouei, A, Mirzaei, M, Fallahzadeh, H
Health education research. 2019;(3):268-278
Abstract
This study was conducted to evaluate an education program based on the theory of planned behavior (TPB) for salt intake in individuals at risk of hypertension. This randomized controlled trial was conducted from February 2017 to December 2017 in Shahediyeh, Yazd Province, Iran. For this purpose, 140 people were selected and assigned to two groups of 70 each, namely, intervention and control. Data were gathered by a self-administered TPB based questionnaire, and also 24-h urinary sodium and potassium levels and systolic and diastolic blood pressure were measured. The intervention group received TPB based on a training package, while the control group received no intervention. Post-test was administered 2 months after completion of the intervention. Independent and paired t-tests, χ2 and analysis of covariance (ANCOVA) were used for data analysis. All mean scores on TPB constructs increased significantly except motivation to comply and power of control for intervention group. Average salt intake decreased in intervention group compared with the control group (-4.73 g/day �0.73 versus -0.24 g/day �0.94, P < 0.001), but systolic and diastolic blood pressure did not change significantly in intervention group compared with control group. TPB can be implemented along with other approaches in educational programs to reduce salt intake. Code: IRCT201701108803N3.
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Salt Reduction Intervention in Families Investigating Metabolic, Behavioral and Health Effects of Targeted Intake Reductions: Study Protocol for a Four Months Three-Armed, Randomized, Controlled "Real-Life" Trial.
Bjoernsbo, KS, Riis, NL, Andreasen, AH, Petersen, J, Dahl Lassen, A, Trolle, E, Frederiksen, AKS, Munk, JK, Toft, U
International journal of environmental research and public health. 2019;(19)
Abstract
Reductions in salt intake have the potential to markedly improve population health at low cost. Real life interventions that explore the feasibility and health effects of a gradual salt reduction lasting at least four weeks are required. The randomized controlled SalT Reduction InterVEntion (STRIVE) trial was developed to investigate the metabolic, behavioral and health effects of four months of consuming gradually salt reduced bread alone or in combination with dietary counselling. This paper describes the rationale and methods of STRIVE. Aiming at 120 healthy families, participants were recruited in February 2018 from the Danish Capital Region and randomly allocated into: (A) Salt reduced bread; (B) Salt reduced bread and dietary counseling; (C) Standard bread. Participants were examined before the intervention and at four months follow-up. Primary outcome is change in salt intake measured by 24 h urine. Secondary outcomes are change in urine measures of potassium and sodium/ potassium ratio, blood pressure, plasma lipids, the renin-angiotensin system, the sympathetic nervous response, dietary intake as well as salt taste sensitivity and preferences. The results will qualify mechanisms affected during a gradual reduction in salt intake in compliance with the current public health recommendations.