EFFECTS OF SHORT-TERM MODIFICATION OF DIETARY SODIUM INTAKE ON PLASMA CATECHOLAMINES AND BLOOD PRESSURE IN PREHYPERTENSIVE CHILDREN

1986 ◽  
Vol 13 (4) ◽  
pp. 305-309 ◽  
Author(s):  
P. R. C. Howe ◽  
P. F. Rogers ◽  
R. M. Smith ◽  
K. F. Jureidini
Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1502
Author(s):  
Katarzyna Łabno-Kirszniok ◽  
Agata Kujawa-Szewieczek ◽  
Andrzej Wiecek ◽  
Grzegorz Piecha

Increased marinobufagenin (MBG) synthesis has been suggested in response to high dietary salt intake. The aim of this study was to determine the effects of short-term changes in sodium intake on plasma MBG levels in patients with primary salt-sensitive and salt-insensitive hypertension. In total, 51 patients with primary hypertension were evaluated during acute sodium restriction and sodium loading. Plasma or serum concentrations of MBG, natriuretic pro-peptides, aldosterone, sodium, potassium, as well as hematocrit (Hct) value, plasma renin activity (PRA) and urinary sodium and potassium excretion were measured. Ambulatory blood pressure monitoring (ABPM) and echocardiography were performed at baseline. In salt-sensitive patients with primary hypertension plasma MBG correlated positively with diastolic blood pressure (ABPM) and serum NT-proANP concentration at baseline and with serum NT-proANP concentration after dietary sodium restriction. In this subgroup plasma MBG concentration decreased during sodium restriction, and a parallel increase of PRA was observed. Acute salt loading further decreased plasma MBG concentration in salt-sensitive subjects in contrast to salt insensitive patients. No correlation was found between plasma MBG concentration and left ventricular mass index. In conclusion, in salt-sensitive hypertensive patients plasma MBG concentration correlates with 24-h diastolic blood pressure and dietary sodium restriction reduces plasma MBG levels. Decreased MBG secretion in response to acute salt loading may play an important role in the pathogenesis of salt sensitivity.


Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Jordan C Patik ◽  
Joseph M Stock ◽  
Nathan T Romberger ◽  
Shannon L Lennon ◽  
William B Farquhar ◽  
...  

Impaired vascular function likely contributes to the association between dietary sodium intake and the development of cardiovascular disease. Using the cutaneous microvasculature as a model, we have previously shown that a high sodium (HS) diet blunts local heating-induced vasodilation in normotensive individuals with salt resistant (SR) blood pressure (BP). However, the effect of a HS diet on the cutaneous microvasculature in normotensive salt sensitive (SS) individuals remains unclear. Therefore, we tested the hypothesis that cutaneous microvascular function is reduced by a HS diet to a greater degree in SS compared to SR individuals. After each 7-day controlled feeding diet (low sodium (LS) = 20 mmol/day; HS = 300 mmol/day), an intradermal microdialysis fiber was inserted in the ventral forearm and perfused with Ringer’s solution. Skin blood flow (SkBF) was continuously monitored via laser Doppler flowmetry and a local heating unit was placed over the fiber and heated to 42°C until SkBF reached a stable plateau. Site-specific maximal SkBF was determined by perfusing 28mM sodium nitroprusside and heating to 43°C. Mean arterial pressure (MAP) was assessed at regular intervals on the contralateral arm and was used to calculate cutaneous vascular conductance (CVC = SkBF / MAP). Subjects wore a 24-hr ambulatory BP monitor and collected their urine on the final day of each diet. Fourteen subjects (9W / 5M, 42 ± 14 yr) whose MAP increased >5 mmHg (Δ8 ± 1 mmHg) on the HS diet were defined as SS and were compared to 14 age- (43± 14 yr) and sex-matched SR subjects (Δ1 ± 3 mmHg). SS and SR had similar MAP at baseline (88 ± 9 vs. 90 ± 8 mmHg, P = 0.88) and urinary sodium excretion was increased similarly across groups by the HS diet (Δ239 ± 104 vs. Δ220 ± 66 mmol / 24 hr, P = 0.20). Cutaneous vasodilation in response to local heating was decreased on the HS diet relative to the LS diet in both SS (Δ-9 ± 9 %CVCmax, P = 0.005) and SR (Δ-9 ± 9 %CVCmax, P=0.005); however, there was not a group x diet interaction (P = 0.99). In contrast to our hypothesis, these results suggest that the deleterious effects of high sodium diets on cutaneous microvascular function are similar in normotensive salt sensitive and salt resistant individuals.


1991 ◽  
Vol 9 (2) ◽  
pp. 181-186 ◽  
Author(s):  
Peter R.C Howe ◽  
Lynne Cobiac ◽  
Richard M. Smith

Circulation ◽  
2021 ◽  
Vol 143 (16) ◽  
pp. 1542-1567 ◽  
Author(s):  
Tommaso Filippini ◽  
Marcella Malavolti ◽  
Paul K. Whelton ◽  
Androniki Naska ◽  
Nicola Orsini ◽  
...  

Background: The relationship between dietary sodium intake and blood pressure (BP) has been tested in clinical trials and nonexperimental human studies, indicating a direct association. The exact shape of the dose–response relationship has been difficult to assess in clinical trials because of the lack of random-effects dose–response statistical models that can include 2-arm comparisons. Methods: After performing a comprehensive literature search for experimental studies that investigated the BP effects of changes in dietary sodium intake, we conducted a dose–response meta-analysis using the new 1-stage cubic spline mixed-effects model. We included trials with at least 4 weeks of follow-up; 24-hour urinary sodium excretion measurements; sodium manipulation through dietary change or supplementation, or both; and measurements of systolic and diastolic BP at the beginning and end of treatment. Results: We identified 85 eligible trials with sodium intake ranging from 0.4 to 7.6 g/d and follow-up from 4 weeks to 36 months. The trials were conducted in participants with hypertension (n=65), without hypertension (n=11), or a combination (n=9). Overall, the pooled data were compatible with an approximately linear relationship between achieved sodium intake and mean systolic as well as diastolic BP, with no indication of a flattening of the curve at either the lowest or highest levels of sodium exposure. Results were similar for participants with or without hypertension, but the former group showed a steeper decrease in BP after sodium reduction. Intervention duration (≥12 weeks versus 4 to 11 weeks), type of study design (parallel or crossover), use of antihypertensive medication, and participants’ sex had little influence on the BP effects of sodium reduction. Additional analyses based on the BP effect of difference in sodium exposure between study arms at the end of the trial confirmed the results on the basis of achieved sodium intake. Conclusions: In this dose–response analysis of sodium reduction in clinical trials, we identified an approximately linear relationship between sodium intake and reduction in both systolic and diastolic BP across the entire range of dietary sodium exposure. Although this occurred independently of baseline BP, the effect of sodium reduction on level of BP was more pronounced in participants with a higher BP level.


Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1970 ◽  
Author(s):  
Grillo ◽  
Salvi ◽  
Coruzzi ◽  
Salvi ◽  
Parati

The close relationship between hypertension and dietary sodium intake is widely recognized and supported by several studies. A reduction in dietary sodium not only decreases the blood pressure and the incidence of hypertension, but is also associated with a reduction in morbidity and mortality from cardiovascular diseases. Prolonged modest reduction in salt intake induces a relevant fall in blood pressure in both hypertensive and normotensive individuals, irrespective of sex and ethnic group, with larger falls in systolic blood pressure for larger reductions in dietary salt. The high sodium intake and the increase in blood pressure levels are related to water retention, increase in systemic peripheral resistance, alterations in the endothelial function, changes in the structure and function of large elastic arteries, modification in sympathetic activity, and in the autonomic neuronal modulation of the cardiovascular system. In this review, we have focused on the effects of sodium intake on vascular hemodynamics and their implication in the pathogenesis of hypertension.


2002 ◽  
Vol 283 (3) ◽  
pp. F447-F453 ◽  
Author(s):  
Amy J. Mangrum ◽  
R. Ariel Gomez ◽  
Victoria F. Norwood

The present study was performed to investigate the role of type 1A ANG II (AT1A) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT1A receptor-deficient (−/−) mice. Groups of AT1A (−/−) and wild-type mice were placed on a low (LS)-, normal (NS)-, or high-salt (HS) diet for 3 wk. AT1A(−/−) mice on an LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On an HS diet, (−/−) mice demonstrated significant diuresis, yet blood pressure increased to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure-natriuresis relationship in AT1A (−/−) mice demonstrated a shift to the left and a decreased slope compared with wild-type littermates. These studies demonstrate that mice lacking the AT1A receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.


2020 ◽  
Vol 41 (35) ◽  
pp. 3363-3373 ◽  
Author(s):  
Martin O’Donnell ◽  
Andrew Mente ◽  
Michael H Alderman ◽  
Adrian J B Brady ◽  
Rafael Diaz ◽  
...  

Abstract Several blood pressure guidelines recommend low sodium intake (<2.3 g/day, 100 mmol, 5.8 g/day of salt) for the entire population, on the premise that reductions in sodium intake, irrespective of the levels, will lower blood pressure, and, in turn, reduce cardiovascular disease occurrence. These guidelines have been developed without effective interventions to achieve sustained low sodium intake in free-living individuals, without a feasible method to estimate sodium intake reliably in individuals, and without high-quality evidence that low sodium intake reduces cardiovascular events (compared with moderate intake). In this review, we examine whether the recommendation for low sodium intake, reached by current guideline panels, is supported by robust evidence. Our review provides a counterpoint to the current recommendation for low sodium intake and suggests that a specific low sodium intake target (e.g. <2.3 g/day) for individuals may be unfeasible, of uncertain effect on other dietary factors and of unproven effectiveness in reducing cardiovascular disease. We contend that current evidence, despite methodological limitations, suggests that most of the world’s population consume a moderate range of dietary sodium (2.3–4.6g/day; 1–2 teaspoons of salt) that is not associated with increased cardiovascular risk, and that the risk of cardiovascular disease increases when sodium intakes exceed 5 g/day. While current evidence has limitations, and there are differences of opinion in interpretation of existing evidence, it is reasonable, based upon observational studies, to suggest a population-level mean target of <5 g/day in populations with mean sodium intake of >5 g/day, while awaiting the results of large randomized controlled trials of sodium reduction on incidence of cardiovascular events and mortality.


1986 ◽  
Vol 64 (6) ◽  
pp. 772-780 ◽  
Author(s):  
George H. Beaton ◽  
Anne Chery

The choice of dietary methodology can affect the ability to detect and describe the relationship between dietary sodium intake and blood pressure. This is illustrated in this paper through the use of simulation modelling of the effect of using different dietary methods (food recalls or records covering different numbers of days, food frequency questionnaire estimates of a single diet component) and using urinary excretion as a proxy for intake. Both epidemiologic studies and experimental interventions are simulated. Although the data base used was simulated rather than real, an attempt was made to keep it realistic in relation to what might be seen in actual populations. From these analyses it can be inferred that with appropriate choice of methodology and study design, even low order relationships between sodium intake and blood pressure should be detectable. At a more general level, it may be concluded that while there is no perfect dietary methodology, there are preferred methodologies for defined purposes.


1997 ◽  
Vol 78 (1) ◽  
pp. 73-82 ◽  
Author(s):  
Georg Lietz ◽  
Alison Avenell ◽  
Simon P Robins

The influence of Na load on bone metabolism was investigated in postmenopausal women using urinary deoxypyridinoline (DPD) as a marker of bone resorption. In a cross-over study, fourteen postmenopausal women were divided into two groups of seven. A fixed diet providing 816 mg Ca/d with either 60 or 170 mmol Na/d was consumed. At the end of an 8 d period the groups switched diets for a further 8d period. Urine was collected daily for the last 4d of each period. There was no significant difference in DPD excretion between high-Na and low-Na diets (129 nmol/d v. 132 nmol/d; P = 0·18). There was, however, a significant relationship (P = 0·02) between the changes in DPD excretion and urinary Ca. Plasma Mg fell from 0·83 to 0·81mmol/l on the high Na intake (P<0·001), but there was no significant effect on plasma Ca or intact parathyroid hormone levels. It is concluded that varying dietary Na intake may affect Ca and Mg metabolism, but we were unable to demonstrate an effect on bone resorption at the levels of intake used


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