Search

BACKGROUND Sodium intake is known to contribute to the development of hypertension, thus intake reduction is a cornerstone in the prevention and management of hypertension. The increase in renal sodium excretion might represent a further potential preventive and/or therapeutic opportunity. OBJECTIVE To explore the working hypothesis that an increased fluid intake can improve renal sodium handling towards a decrease in blood pressure. METHODS The SPA Project is a multicenter, observational, cross-sectional, cohort study investigating healthy children, aged 5-8 years as to sodium and fluid intake by means of urinary sodium and creatinine from multiple samples taken in different days in order to characterize them in lower/higher sodium and lower/higher fluid intake. Both SBP and DBP (by multiple office blood pressure measurements) were used as outcome measures. RESULTS Three hundred and thirty-nine healthy, nonoverweight children (51.6% boys) with a median age of 5.7 years old (IQR: 5.3-6.2) participated in the study but only 223 could be analyzed. Among children with higher sodium intake, those introducing more fluids, showed a significantly lower blood pressure (both systolic and diastolic) compared with those with lower fluid intake: systolic 86.0 ± 8.5 vs. 90.0 ± 8.1 mmHg; P = 0.014 and diastolic: 53.8 ± 4.9 vs. 58.6 ± 6.6 mmHg; P

Objective This study conducted exploratory metabolomic and lipidomic profiling of plasma samples from the DASH (Dietary Approaches to Stop Hypertension) Sodium Trial to identify unique plasma biomarkers to identify salt-sensitive versus salt-resistant participants. Methods Utilizing plasma samples from the DASH-Sodium Trial, we conducted untargeted metabolomic and lipidomic profiling on plasma from salt-sensitive and salt-resistant DASH-Sodium Trial participants. Study 1 analyzed plasma from 106 salt-sensitive and 85 salt-resistant participants obtained during screening when participants consumed their regular diet. Study 2 examined paired within-participant plasma samples in 20 salt-sensitive and 20 salt-resistant participants during a high-salt and low-salt dietary intervention. To investigate differences in metabolites or lipidomes that could discriminate between salt-sensitive and salt-resistant participants or the response to a dietary sodium intervention Principal Component Analysis and Orthogonal Partial Least Square Discriminant Analysis was conducted. Differential expression analysis was performed to validate observed variance and to determine the statistical significance. Results Differential expression analysis between salt-sensitive and salt-resistant participants at screening revealed no difference in plasma metabolites or lipidomes. In contrast, three annotated plasma metabolites, tocopherol alpha, 2-ketoisocaproic acid, and citramalic acid, differed significantly between high-sodium and low-sodium dietary interventions in salt-sensitive participants. Conclusion In DASH-Sodium Trial participants on a regular diet, plasma metabolomic or lipidomic signatures were not different between salt-sensitive and salt-resistant participants. High-sodium intake was associated with changes in specific circulating metabolites in salt-sensitive participants. Further studies are needed to validate the identified metabolites as potential biomarkers that are associated with the salt sensitivity of blood pressure.

Although most current guidelines recommend a daily sodium intake of less than 2.3 g/day, most people do not have a reliable estimate of their usual sodium intake. In this review, we describe the different methods used to estimate sodium intake and discuss each method in the context of specific clinical or research questions. We suggest the following classification for sodium measurement methods: preingestion measurement (controlled intake), peri-ingestion measurement (concurrent), and postingestion measurement. On the basis of the characteristics of the available tools, we suggest that: validated 24-h recall methods are a reasonable approach to estimate sodium intake in large epidemiologic studies and individual clinical counselling sessions, methods (such as single 24-h urine collection, single-time urine collection, or 24-h recall methods), are of value in population-level estimation of mean sodium intake, but are less suited for individual level estimation and a feeding-trial design using a controlled diet is the most valid and reliable method for establishing the effect of reducing sodium to a specific intake target in early phase clinical trials. By considering the various approaches to sodium measurement, investigators and public health practitioners may be better informed in assessing the health implications of sodium consumption at the individual and population level.

Objective: The objective was to evaluate the accuracy of five formulas -- the Kawasaki, Tanaka, INTERSALT, Mage, and Uechi methods -- using spot urinary sampling for 24-h urinary sodium (UNa) prediction in hypertensive patients living in northeast China. Methods: There were 1154 hypertensive patients enrolled from multiple centers. Five different formulas were used to predict 24-h UNa excretion via spot morning urinary samples. Actual UNa excretion was measured from 24-h urine samples. The estimated value was compared with the actual value by examining biases, the intraclass correlation coefficients (ICC), and Bland–Altman plots. Results: The average excretion of sodium was 2.97 ± 1.26 g/day. The formula-produced mean biases for actual UNa were 0.31 g/day for INTERSALT, 0.80 g/day for Mage, 0.88 g/day for Tanaka, 1.14 g/day for Uechi, and 1.95 g/day for Kawasaki. The ICC was 0.511 for Kawasaki, 0.499 for INTERSALT, 0.468 for Tanaka, 0.402 for Mage, and 0.378 for Uechi. The least mean bias in the lower and moderate salt intake subgroups was 1.22 and 0.07 g/day, respectively, which was calculated using the Mage and INTERSALT methods. The least mean bias in the higher salt intake subgroup was 0.10 g/day for the Uechi method. The INTERSALT method was more efficiency at the individual level, with 17.4% of participants having relative differences within 10%, and 22.3% participants having absolute differences within 393 mg. Conclusion: The INTERSALT method may exhibit a good performance in estimating 24-h urinary sodium level for the hypertensive population living in northeast China.

Objective: Our aim was to analyze sodium and potassium intake in obese normotensive and hypertensive subjects from rural area. Design and method: Out of 1582 subjects (random rural sample) enrolled in ENAH study conducted in 2008–2010, 739 were invited for the second visit in 2015 and 377 subjects with reliable both urine samples (urine creatinine in normal ranges) were included in further analyses s (80m 297w ; average age 52 ± 13.5). Blood pressure was measured three times (Omron M6) and mean values were calculated. Fasting blood and first morning (spot) urine samples were collected. Sodium and potassium were determined using Tanaka, Kawasaki and Intersalt equations. Potassium intake was further adjusted for intestinal intake (77%) and renal excretion (92%). Optimal, normal, high normal BP, untreated and treated hypertension (HT) were diagnosed in 20.9%, 15.3%, 12.9%, 19.1% and 31.5%, respectively. There were 21.2%, 35.3% and 42.8% subjects in the BMI 1 (30) group, respectively. Results: Significant differences in HT prevalence were observed among the BMI groups (46.9%, 63.6%, 80 %, respectively ; p = 0.001). Sodium excretion were significantly lower in BMI1 vs BMI3 groups (BMI < 0.0001). More than 10 g/day of salt intake was most seldom present in BMI1 and more frequently in BMI3 group (41.9%, 54.5%, 63.1%, respectively ; p < 0.05). Compared to normotensive in hypertensive subjects salt intake >10 g/day was significantly more frequently presented in overweight (X2 = 12.68 ; p = 0.0003) but not in obese subjects. Potassium intake was significantly higher in BMI3 than in BMI1 group (p < 0.001). No differences in Na/K ratio were observed among BMI groups. Conclusions: Higher salt intake contributes to high prevalence of hypertension and according to our results is more closely associated with hypertension in overweight than in obese subjects. No difference in Na/K ratio among BMI groups reflects high sodium and poor potassium intake in all subjects.

Objective:Disaster hypertension has been considerd to be one of the most contributions to the occurrence of cardiovascular events after disaster. Although there was association between sodium intake and blood pressure (BP) in usual state, data are sparse about the association between salt-intake and

Arterial stiffness is an independent cardiovascular risk factor and sodium intake could be a determinant of arterial stiffness. Nevertheless, the studies that investigated the effect of reducing dietary sodium intake on arterial stiffness in humans provided inconsistent results. Therefore, we performed a systematic review and a meta-analysis of the available randomized controlled trials of salt restriction and arterial stiffness to try and achieve more definitive conclusions. A systematic search of the online databases available (from 1996 through July 2017) was conducted including randomized controlled trials that reported arterial stiffness, expressed by carotid–femoral pulse wave velocity (PWV), as difference between the effects of two different sodium intake regimens. For each study, the mean difference and 95% confidence intervals were pooled using a random effect model. Sensitivity, heterogeneity, publication bias, subgroup and meta-regression analyses were performed. Eleven studies met the predefined inclusion criteria and provided 14 cohorts with 431 participants and 1–6 weeks intervention time. In the pooled analysis, an average reduction in sodium intake of 89.3 mmol/day was associated with a 2.84% (95% CI: 0.51–5.08) reduction in PWV. There was no significant heterogeneity among studies and no evidence of publication bias was detected. No single feature of the studies analyzed seemed to impact on the effect of salt restriction on PWV. The results of this meta-analysis indicate that restriction of dietary sodium intake reduces arterial stiffness. This effect seems be at least in part independent of the changes in blood pressure.

Objectives:To study the associations between sodium intake and target organ damage in patients with refractory hypertension (RH).Methods:We consecutively recruited 147 RH patients (47.6% male, age 54.14 ± 16.15 years) who took at least three antihypertensive drugs including diuretics. 24-hour urinar

Objectives:Sodium intake is rarely monitored in clinical practice although it has been associated with blood pressure and antihypertensive drugs. 24-hour urine collection for sodium excretion is the most reliable method in estimating sodium intake, but the method is rather cumbersome. Thus this stud

Aldosterone-to-renin ratio (ARR) is an index for inappropriate aldosterone activity and salt sensitivity. We previously reported that elevated ARR might be associated with salt-sensitive hypertension. Because salt-sensitive hypertensive patients are reported to show a diminished nocturnal decline in blood pressure, we hypothesized that high ARR may be associated with diminished nocturnal decline in blood pressure (generally referred to as a 'nondipping' pattern), especially in individuals with high sodium intake.This study tested this hypothesis in 184 participants aged at least 55 years not receiving antihypertensive treatment in a general Japanese population (age: 67.6 ± 6.9 years; 71.7% women).Ambulatory blood pressure monitoring identified 63 (34.2%) participants with a nondipping pattern (nocturnal decline of SBP10%). The median plasma renin activity (PRA), plasma aldosterone concentration (PAC), and ARR were 0.8 ng/ml per h, 8.3 ng/dl, and 8.7 ng/dl per (ng/ml per h), respectively. After adjustment for possible confounding factors, each 1 SD increase in logARR was associated with the prevalence of nondipping pattern (odds ratio, 1.95; P = 0.002). This association was observed in individuals in the highest tertile of 24-h urinary sodium excretion estimated from spot urine data (e24-hUNa; ≥179.6 mEq/day; P = 0.01) but disappeared in those in the lowest tertile of e24-hUNa (147.9 mEq/day; P = 0.6). In those in the highest tertile of e24-hUNa, PRA was significantly lower in nondippers than in dippers (0.49 vs. 0.85 ng/ml per h) despite no differences in PAC.These results suggest that relative aldosterone excess might be related to a nondipping pattern of blood pressure, especially in individuals with high sodium intake.

To guide resource allocation, policy makers need evidence of the cost-effectiveness of interventions. We summarized such evidence on selected interventions to reduce sodium intake that would be intended as population-wide approaches to control hypertension.We conducted a comprehensive literature review of journal articles published in English from January 2000 to May 2010 by searching the databases of PubMed, EMBASE, MEDLINE, and EconLit. We selected original research articles for abstracting the evidence on cost-effectiveness of interventions, cost savings and the costs of intervention implementation.From the 53 references obtained from the literature search, we identified 11 original research articles that provided relevant information on the medical cost savings, implementation costs, or cost-effectiveness of interventions to reduce sodium intake. The interventions were low in cost, e. g., one study showed that the cost ranged from US$ 0.03 to 0.32 per person per year for awareness campaign through mass media outlets and government regulations on food products in low and middle-income countries. Population-wide interventions for salt reduction are very cost-effective such as only ARS$ 151 per disability-adjusted life-year (DALY) saved in Argentina, whereas statin therapy to lower high cholesterol was $ 70,994 per DALY saved. Another study showed that sodium reduction could save US$ 18 billion in annual US healthcare costs by reducing sodium intake to 2300 mg/day.The literature provided economic evidence that was in favor of population-wide interventions designed to reduce sodium intake. Reducing the intake of sodium through such initiatives might be one of the best buys in public health. However, the small body of literature and hypothetical scenarios in most studies might limit policy implications of the findings.

Background Renin-angiotensin-aldosterone system blockade is a cornerstone in cardiovascular protection. Angiotensin-converting enzyme (ACE)-DD genotype has been associated with resistance to angiotensin-converting enzyme inhibition (ACEi), but data are conflicting. As sodium intake modifies the effect of ACEi as well as the genotype-phenotype relationship, we hypothesize gene-environment interaction between sodium-status, the response to ACEi, and ACE genotype. Method Thirty-five male volunteers (26 +/- 9 years; II n=6, ID n=18, DD n=11) were studied during placebo and ACEi (double blind, enalapril 20mg/day) on low [7 days 50 mmol Na+/day (low salt)] and high[7 days 200 mmol Na+/day (high salt)] sodium, with a washout of 6 weeks in-between. After each period mean arterial pressure (MAP) was measured before and during graded infusion of angiotensin II (Ang II). Results During high salt, ACEi reduced MAP in II and ID, but not in DD [II: 88 (78-94) versus 76 (72-88); ID: 87 (84-91) versus 83 (79-87); both P Conclusion In healthy participants, the MAP response to ACEi is selectively blunted in DD genotype during high salt, accompanied by blunted sensitivity to Ang II. Low salt corrects both abnormalities. Further analysis of this gene-environment interaction in patients may contribute to strategies for improvement of individual treatment efficacy. J Hypertens 28:2414-2421 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

Background Renin-angiotensin-aldosterone system blockade is a cornerstone in cardiovascular protection. Angiotensin-converting enzyme (ACE)-DD genotype has been associated with resistance to angiotensin-converting enzyme inhibition (ACEi), but data are conflicting. As sodium intake modifies the effect of ACEi as well as the genotype-phenotype relationship, we hypothesize gene-environment interaction between sodium-status, the response to ACEi, and ACE genotype.Method Thirty-five male volunteers (26 +/- 9 years; II n=6, ID n=18, DD n=11) were studied during placebo and ACEi (double blind, enalapril 20mg/day) on low [7 days 50 mmol Na+/day (low salt)] and high[7 days 200 mmol Na+/day (high salt)] sodium, with a washout of 6 weeks in-between. After each period mean arterial pressure (MAP) was measured before and during graded infusion of angiotensin II (Ang II).Results During high salt, ACEi reduced MAP in II and ID, but not in DD [II: 88 (78-94) versus 76 (72-88); ID: 87 (84-91) versus 83 (79-87); both PConclusion In healthy participants, the MAP response to ACEi is selectively blunted in DD genotype during high salt, accompanied by blunted sensitivity to Ang II. Low salt corrects both abnormalities. Further analysis of this gene-environment interaction in patients may contribute to strategies for improvement of individual treatment efficacy. J Hypertens 28:2414-2421 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

To assess the trends in blood pressure (BP) affecting lifestyle factors in hypertensive and normotensive Finns from 1982 to 2002.Five independent cross-sectional population surveys conducted in 1982, 1987, 1992, 1997 and 2002 in the provinces of North Karelia and Kuopio in eastern Finland and the region of Turku-Loimaa in southwestern Finland.Stratified random samples of men and women aged 25-64 years were drawn from the national population register. The participants (n = 28 235) were classified into four groups according to their BP level and treatment status: normotensive, unaware hypertensive, aware but untreated hypertensive, and treated hypertensive subjects.Alcohol intake, body mass index (BMI), 24-h urinary sodium and potassium excretion (a subsample of 5849 subjects) and the proportion of subjects with leisure-time physical activity (LTPA) at least three times a week.Mean BMI increased significantly in all groups except in untreated hypertensive women. Alcohol intake increased in all men but especially in hypertensive women (P0.001). The 24-h urinary sodium excretion decreased significantly in all BP groups. The proportion of subjects with a recommended level of LTPA increased significantly and similarly in all BP groups (P0.001).The unfavourable trends observed in mean BMI and alcohol intake in the entire population should be reversed in order to decrease the frequency of hypertension in Finland. The health behaviours of hypertensive subjects should be carefully monitored and modified in a more systematic and efficient way than at present.

To examine the interaction of sodium intake with genetic variations of the angiotensinogen gene and hypertension.A community-based case-reference study.Two rural Japanese communities.Non-overweight and non-drinking Japanese men and women: 229 hypertensives and 229 age-, sex- and community-matched normotensives aged 32 to 83 years.Polymorphisms of the angiotensinogen gene detected by an allele-specific polymerase chain reaction. A priori hypothesis is individuals with 174M (threonine-to-methionine substitution) or 235T (methionine-to-threonine substitution) allelic variations may have an elevated risk of hypertension when they have a high sodium intake, estimated by 24-h urine collection and a dietary questionnaire.The genotypic frequency of the haplotype including both the 174M and 235T alleles was higher among hypertensives than among normotensives (23 versus 14%, P= 0.02). The frequency of the 174M allele was specifically higher among hypertensives than normotensives (12 versus 7%, P=0.01), and the odds ratio of hypertension associated with the 174M (versus 174T) allele was 1.8 [95% confidence interval (CI) 1.1-3.0, P=0.01]. The frequency of the 235T allele did not vary between the two groups (80 versus 82%, P= 0.40). The relationship between the 174M allele and hypertension was more evident among persons who had higher urinary sodium excretion (= 166 mmol/day) than those with lower excretion (166 mmol/day): odds ratio 2.5 (95% CI, 1.2-5.2), P=0.01 versus 1.5 (95% CI, 0.7-3.1), P= 0.31; P for interaction = 0.04, and this trend was primarily observed for early-onset hypertension (55 years at onset). A similar but nonsignificant association was observed when stratified using present and past sodium intake scores derived from questionnaires.Angiotensinogen genotype may affect the development of early-onset hypertension among Japanese, particularly in those who have a high sodium intake.

Objective:Increased potassium intake has been related to improved endothelial function and a high sodium intake is known to impair endothelial function. The effect of increasing potassium in the presence of high sodium in the postprandial state is not known. The aim was to determine the effect of in

Objective:We evaluated the influence of sodium intake on aortic pulse wave velocity (PWV).Design and method:Thirty-one hypertensives and 70 normotensives were given 7 days of low sodium dietary approach to stop hypertension (DASH) diet (LSD, 100 mmol NaCl/day) and 7 days of high sodium DASH diet (HS

The contribution of salt intake to the pathogenesis of hypertension holds longstanding interest. Recent studies employed the sensitivity of blood pressure (BP) to salt intake as an intermediate phenotype. The validity of this approach relative to the homogeneity of sodium-sensitive hypertension was investigated while simultaneously controlling multiple putative factors.Blood pressure responses to shifts in salt intake were measured in 274 individuals with essential hypertension in steady-state sodium balance on high (200 mEq) and low (10 mEq) sodium intakes. Univariate and multivariate analyses predicted systolic and diastolic sodium sensitivity based on interactions among demographic factors (age, gender, race, body mass index) and hypertensive type [low-renin (LR), modulator (M), non-modulator (NM)].The influence of hypertension type on systolic salt sensitivity (SSS) depended on gender (P = 0.03). In females, highest SSS was in LR (21, 14, 13 mmHg for LR, M, NM, P = 0.02), while in males highest SSS was in NM (11, 10, 16 mmHg for LR, M, NM, P = 0.07). Age predicted SSS without interacting with other factors, producing a 2.4 mmHg increase per decade (P = 0.02). Hypertension type affected diastolic salt sensitivity (DSS) (P = 0.002) without interacting with other factors. M had less DSS (6 mmHg) than LR (9 mmHg) and NM (11 mmHg) (P0.01).For subjects in sodium balance, the distributions of SSS and DSS were unimodal and the mechanisms mediating SSS and DSS were different. Controlling for multiple demographic factors, at least two hypertensive types have largest BP responses to sodium intake, reducing the usefulness of blood pressure sensitivity to salt intake as an intermediate phenotype.

Although the concept of the pressure-natriuresis curve is very clear, considerable confusion concerning its importance and utility in understanding the pathophysiology of hypertension persists. We recently showed that the pressure-natriuresis curve could be considered linear. In this brief review, we would like to stress the advantages of treating it as a line. Its linear approximation simplifies understanding of the sodium sensitivity of the blood pressure and mechanisms of hypertension. The blood pressure can be expressed as the sum of two components: the non-sodium-sensitive component determined by the x intercept of the pressure-natriuresis curve and the sodium sensitive one determined by the product of the reciprocal of the slope and the amount of sodium intake. Theoretically, it can be affected in two different ways to cause hypertension; either a parallel shift along the blood pressure axis toward a higher blood pressure level due to the increase in the x intercept or a decrease in the slope. The parallel shift induces non-sodium-sensitive hypertension, whereas the decrease in slope induces sodium-sensitive hypertension. Thus, the linear approximation makes the definition of the sodium sensitivity of the blood pressure very clear and, furthermore, suggests that mechanisms of hypertension can be clarified if the determinants of the x intercept and the slope of the pressure-natriuresis curve are known. A clear definition of sodium sensitivity allows us to study its importance as a marker of a greater risk of renal and cardiovascular complications.

Among the many factors that have been implicated in the pathogenesis of myocardial hypertrophy is a sodium effect. In the present study, the influence of dietary sodium, estimated by 24-h natriuresis, on left ventricular mass was assessed in 41 patients with mild essential hypertension who had never been treated. Posterior wall thickness and left ventricular mass, but not left ventricular internal diameter were directly correlated with 24-h natriuresis (r = 0.47 and 0.46; P less than 0.02 and 0.002, respectively). Stepwise multiple regression analysis confirmed that 24-h natriuresis was a determinant of left ventricular mass independently of sex, age, body weight, blood pressure and the duration of hypertension. These results suggest that dietary sodium may play a role in modulating left ventricular mass in untreated hypertensives.