The Impact of High Dietary Sodium Consumption on Blood Pressure Variability in Healthy, Young Adults

Abstract BACKGROUND High sodium (Na+) intake augments blood pressure variability (BPV) in normotensive rodents, without changes in resting blood pressure (BP). Augmented BPV is associated with end-organ damage and cardiovascular morbidity. It is unknown if changes in dietary Na+ influence BPV in humans. We tested the hypothesis that high Na+ feeding would augment BPV in healthy adults. METHODS Twenty-one participants (10 F/11 M; 26 ± 5 years; BP: 113 ± 11/62 ± 7 mm Hg) underwent a randomized, controlled feeding study that consisted of 10 days of low (2.6 g/day), medium (6.0 g/day), and high (18.0 g/day) salt diets. On the ninth day of each diet, 24-h urine samples were collected and BPV was calculated from 24-h ambulatory BP monitoring. On the tenth day, in-laboratory beat-to-beat BPV was calculated during 10 min of rest. Serum electrolytes were assessed. We calculated average real variability (ARV) and standard deviation (SD) as metrics of BPV. As a secondary analysis, we calculated central BPV from the 24-h ambulatory BP monitoring. RESULTS 24-h urinary Na+ excretion (low = 41 ± 24, medium = 97 ± 43, high = 265 ± 92 mmol/24 h, P < 0.01) and serum Na+ (low = 140.0 ± 2.1, medium = 140.7 ± 2.7, high = 141.7 ± 2.5 mmol/l, P = 0.009) increased with greater salt intake. 24-h ambulatory ARV (systolic BP ARV: low = 9.5 ± 1.7, medium = 9.5 ± 1.2, high = 10.0 ± 1.9 mm Hg, P = 0.37) and beat-to-beat ARV (systolic BP ARV: low = 2.1 ± 0.6, medium = 2.0 ± 0.4, high = 2.2 ± 0.8 mm Hg, P = 0.46) were not different. 24-h ambulatory SD (systolic BP: P = 0.29) and beat-to-beat SD (systolic BP: P = 0.47) were not different. There was a trend for a main effect of the diet (P = 0.08) for 24-h ambulatory central systolic BPV. CONCLUSIONS Ten days of high sodium feeding does not augment peripheral BPV in healthy, adults. CLINICAL TRIALS REGISTRATION NCT02881515.

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Sodium Intake and Hypertension

Nutrients ◽

10.3390/nu11091970 ◽

2019 ◽

Vol 11 (9) ◽

pp. 1970 ◽

Cited By ~ 28

Author(s):

Grillo ◽

Salvi ◽

Coruzzi ◽

Salvi ◽

Parati

Keyword(s):

Blood Pressure ◽

Salt Intake ◽

Sodium Intake ◽

Peripheral Resistance ◽

Dietary Sodium ◽

Dietary Salt ◽

High Sodium ◽

Close Relationship ◽

And Function ◽

Modest Reduction

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.

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Association of Urinary Sodium Excretion with Vascular Damage: A Local Kidney Effect, Rather Than a Marker of Generalized Vascular Impairment

International Journal of Hypertension ◽

10.1155/2018/7620563 ◽

2018 ◽

Vol 2018 ◽

pp. 1-7 ◽

Cited By ~ 2

Author(s):

Areti Triantafyllou ◽

Panagiota Anyfanti ◽

Eugenia Gkaliagkousi ◽

Xenophon Zabulis ◽

Anastasios Vamvakis ◽

...

Keyword(s):

Blood Pressure ◽

Arterial Stiffness ◽

Sodium Excretion ◽

Salt Intake ◽

Augmentation Index ◽

Urinary Sodium Excretion ◽

Capillary Density ◽

Organ Damage ◽

Salt Consumption ◽

Ambulatory Bp Monitoring

Evidence suggests that increased salt consumption induces blood pressure- (BP) mediated organ damage, yet it remains unclear whether it reflects a generalized micro- and macrovascular malfunction independent of BP. We studied 197 newly diagnosed and never-treated individuals with hypertension, intermediate hypertensive phenotypes, and normal BP, classified by use of 24-hour ambulatory BP monitoring. Sodium excretion and microalbuminuria were estimated in 24-hour urine samples, dermal capillary density was estimated from capillaroscopy, and arterial stiffness was estimated with pulse wave velocity (PWV) and augmentation index (AIx). Sodium excretion correlated with microalbuminuria (p<0.001) and 24-hour and day- and nighttime systolic BP, but not with office blood pressure, arterial stiffness, or capillary density. In the multivariate analysis, the association with microalbuminuria was maintained (p=0.007). In a population free from the long-standing effects of hypertension, increased salt intake appears to be associated with early signs of vascular kidney damage, rather than a diffuse micro- and macrovascular impairment.

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Dietary Sodium Restriction in the Management of Chronic Kidney Disease: A Systematic Review and Meta-Analysis of RCTs

10.21203/rs.3.rs-806377/v1 ◽

2021 ◽

Author(s):

Sai Sidharth Manikandan ◽

Murali Dhar

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Salt Intake ◽

Sodium Intake ◽

Meta Analysis ◽

Cost Effective ◽

Mean Difference ◽

Dietary Sodium ◽

High Sodium

Abstract Background: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve chronic kidney disease (CKD) prognosis. We decided to perform a meta-analysis of randomized controlled trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Results:Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated glomerular filtration rate (eGFR), however the same was not statistically significant.Conclusion:The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.

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Correlation among high salt intake, blood pressure variability, and target organ damage in patients with essential hypertension

Medicine ◽

10.1097/md.0000000000019548 ◽

2020 ◽

Vol 99 (14) ◽

pp. e19548

Author(s):

Wei Cai ◽

MingJian Lang ◽

XiaoBo Jiang ◽

Qian Yu ◽

Congliang Zhou ◽

...

Keyword(s):

Blood Pressure ◽

Essential Hypertension ◽

Blood Pressure Variability ◽

Salt Intake ◽

Target Organ Damage ◽

Organ Damage ◽

Target Organ ◽

High Salt ◽

High Salt Intake

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Új szempontok a sószenzitív hypertoniák patomechanizmusában

Orvosi Hetilap ◽

10.1556/650.2019.31308 ◽

2019 ◽

Vol 160 (2) ◽

pp. 43-49

Author(s):

Endre Sulyok

Keyword(s):

Blood Pressure ◽

Extracellular Space ◽

Salt Intake ◽

Sodium Intake ◽

Organ Damage ◽

Blood Pressure Elevation ◽

High Sodium ◽

End Organ Damage ◽

Inactive Form ◽

Factor C

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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Abstract P206: Increased Short-term Dietary Sodium Intake Does Not Increase Blood Pressure or Measures of Aortic Stiffness in Young Healthy Adults

Hypertension ◽

10.1161/hyp.68.suppl_1.p206 ◽

2016 ◽

Vol 68 (suppl_1) ◽

Author(s):

Hannah Rosenblum ◽

Stuart Katz

Keyword(s):

Blood Pressure ◽

Young Adults ◽

Pulse Pressure ◽

Repeated Measures ◽

Aortic Stiffness ◽

Healthy Adults ◽

Dietary Sodium ◽

Short Term ◽

Serum Aldosterone ◽

The Impact

Background: Sodium (Na) sensitivity is defined as the short-term increase in blood pressure (BP) after increased Na intake. The impact of Na sensitivity on measures of aortic stiffness has not been previously characterized in non-hypertensives. We tested the feasibility of an oral Na loading protocol to characterize the effects of increased dietary Na on blood pressure and measures of aortic stiffness in health young adults. Methods: In an open-label repeated measures pilot study, we enrolled 40 healthy adults age 21-30 years (18 females). Subjects were evaluated before and after 7 days of oral Na loading (12g (205 mmol) of salt tablets/day). BP (mmHg, cuff method) was measured in supine, seated and standing positions. Radial artery tonometry (Sphygmacor) was used to assess measures of aortic stiffness: aortic BP (mmHg), aortic pulse pressure (mmHg), aortic augmentation index (%) and adjusted Tr, time of return of the reflected pressure wave as an index of aortic pulse wave velocity (m/s). Serum aldosterone, urine Na and potassium (K) were measured. Results: Nine subjects dropped out due to GI intolerance of the salt pills. In the remaining 31 subjects, Na loading did not change BP in any position, aortic BP, aortic pulse pressure, or Tr (Table: mean±SD for seated R arm BP and measures of aortic stiffness). There was no measurable aortic augmentation in the cohort. Na loading decreased serum aldosterone (9.1±1.5 to 5.2±0.8 ng/dl, p=0.02), and increased urine Na:K ratio (1.8±0.2 to 3.5±0.5, p=0.002). Conclusion: Oral Na loading was associated with suppression of the renin-angiotensin aldosterone system, did not increase BP, or measures of aortic stiffness in healthy young adults.

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Dietary Sodium Restriction in the Management of Chronic Kidney Disease: A Meta-Analysis of RCTs

Austin Journal of Nephrology and Hypertension ◽

10.26420/austinjnephrolhypertens.2021.1098 ◽

2021 ◽

Vol 8 (2) ◽

Author(s):

Sai Sidharth M ◽

◽

Dhar M ◽

Keyword(s):

Blood Pressure ◽

Chronic Kidney Disease ◽

Kidney Disease ◽

Salt Intake ◽

Sodium Intake ◽

Meta Analysis ◽

Mean Difference ◽

Dietary Sodium ◽

Cochrane Library ◽

High Sodium

Introduction: Non-pharmacological strategies such as lowering sodium intake aim to protect renal function and delay the initiation of renal replacement therapy. It might also be a cost-effective method to improve Chronic Kidney Disease (CKD) prognosis. We decided to perform a meta-analysis of Randomized Controlled Trials (RCTs) to evaluate the effects of low versus high sodium intake in adults with CKD. Methodology: We searched the online databases – PUBMED, Cochrane Kidney and Transplant Specialized Register, Cochrane Library and Google Scholar to 31st December 2020 for RCTs to be included in the study. Meta- Analysis was performed for the intervention groups for each arm against the control. Inverse variance methods were applied for analysis using random effects models due to the high heterogeneity among the studies. Results: Our search strategy yielded seven studies from six countries with 465 participants. The overall effect on restricted sodium intake favored reduction in systolic blood pressure with an overall mean difference of -6.14(95% CI: -9.52, -2.76) and reduction in diastolic blood pressure with a mean difference of -3.08 (95% CI: -4.62, -1.55). There was lowering of estimated Glomerular Filtration Rate (eGFR), however the same was not statistically significant. Conclusion: The study found that restricted salt intake could significantly reduce systolic and diastolic BP. Further, multi-center RCTs for longer durations across different stages of CKD could effectively assess the effects of restricted sodium intake on vital parameters. Such study designs could also help clinicians identify the optimal intake of dietary sodium to achieve better renal and cardio vascular outcomes.

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Mechanisms of Dietary Sodium-Induced Impairments in Endothelial Function and Potential Countermeasures

Nutrients ◽

10.3390/nu13010270 ◽

2021 ◽

Vol 13 (1) ◽

pp. 270

Author(s):

Jordan C. Patik ◽

Shannon L. Lennon ◽

William B. Farquhar ◽

David G. Edwards

Keyword(s):

Blood Pressure ◽

Endothelial Function ◽

Sodium Intake ◽

Dietary Sodium ◽

Antioxidant Defenses ◽

Endothelial Glycocalyx ◽

Vascular Effects ◽

High Sodium ◽

Cardiovascular Morbidity And Mortality ◽

The Impact

Despite decades of efforts to reduce sodium intake, excess dietary sodium remains commonplace, and contributes to increased cardiovascular morbidity and mortality independent of its effects on blood pressure. An increasing amount of research suggests that high-sodium diets lead to reduced nitric oxide-mediated endothelial function, even in the absence of a change in blood pressure. As endothelial dysfunction is an early step in the progression of cardiovascular diseases, the endothelium presents a target for interventions aimed at reducing the impact of excess dietary sodium. In this review, we briefly define endothelial function and present the literature demonstrating that excess dietary sodium results in impaired endothelial function. We then discuss the mechanisms through which sodium impairs the endothelium, including increased reactive oxygen species, decreased intrinsic antioxidant defenses, endothelial cell stiffening, and damage to the endothelial glycocalyx. Finally, we present selected research findings suggesting that aerobic exercise or increased intake of dietary potassium may counteract the deleterious vascular effects of a high-sodium diet.

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Soybean proteins counteract heart remodeling in wistar rats fed a high sodium chloride diet

Nephrology (Saint-Petersburg) ◽

10.36485/1561-6274-2019-236-92-99 ◽

2019 ◽

Vol 23 (6) ◽

pp. 92-99

Author(s):

I. G. Kayukov ◽

O. N. Beresneva ◽

M. M. Parastaeva ◽

G. T. Ivanova ◽

A. N. Kulikov ◽

...

Keyword(s):

Blood Pressure ◽

Sodium Chloride ◽

Cardiac Remodeling ◽

Wistar Rats ◽

Salt Intake ◽

Left Ventricular ◽

High Salt ◽

Soy Proteins ◽

High Sodium ◽

Heart Remodeling

BACKGROUND. Increased salt intake is associated with a number of cardiovascular events, including increased blood pressure (BP) and the development of left ventricular hypertrophy (LVH). However, there is much evidence that a high content of sodium chloride in the diet does not always lead to an increase in BP, but almost inevitably causes cardiac remodeling, in particular, LVH. Many aspects of myocardial remodeling induced by high sodium content in the food have not been studied enough. THE AIM of the study was to trace the echocardiographic changes in Wistar rats fed the high salt ration and the high salt ration supplemented with soy proteins.MATERIAL AND METHODS. Echocardiography and BP measurements were performed on male Wistar rats, divided into three groups. The first (control; n = 8) included rats that received standard laboratory feed (20.16 % animal protein and 0.34 % NaCl); the second (n = 10) – animals that received standard feed and 8 % NaCl (high salt ration). The third group (n = 10) consisted of rats who consumed a low-protein diet containing 10 % soy protein isolate (SUPRO 760) and 8 % NaCl. The follow-up period was 2 and 4 months.THE RESULTS of the study showed that: (1) the intake of a large amount of salt with a diet does not necessarily lead to the formation of arterial hypertension; (2) despite the absence of a distinct increase in BP, under these conditions signs of cardiac remodeling, in particular, LVH, appear rather quickly; (3) supplementing a high-salt diet with soy isolates counteracts the development of LVH.CONCLUSION. High salt intake with food can cause heart remodeling, regardless of blood pressure, while soy proteins can counteract this process.

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Prevalence, Biochemical and Clinical Characteristics of Resistant Hypertension

Revista de Chimie ◽

10.37358/rc.18.10.6637 ◽

2018 ◽

Vol 69 (10) ◽

pp. 2845-2849

Author(s):

Daniela Gurgus ◽

Elena Ardeleanu ◽

Carmen Gadau ◽

Roxana Folescu ◽

Ioan Tilea ◽

...

Keyword(s):

Blood Pressure ◽

Cardiovascular Disease ◽

Resistant Hypertension ◽

Clinical Characteristics ◽

Salt Intake ◽

Target Organ Damage ◽

Multivariate Logistic Regression Analysis ◽

Organ Damage ◽

Left Ventricular ◽

High Salt Intake

The objectives of the present study were to evaluate the prevalence of resistant hypertension (RH) in primary care setting and to analyse its biochemical and clinical characteristics. After 3 months of treatment and evaluation, 721 (14.01%) of 5,146 patients with hypertension did not reach target office blood pressure of [ 140/90 mmHg. After exclusion of �white-coat effect� with ambulatory blood pressure, of secondary and pseudo- resistant hypertension, prevalence of RH was 6.74%. Lifestyle factors associated with RH were physical inactivity, obesity, high salt intake, smoking and excessive alcohol ingestion. Compared to controlled hypertension, RH patients presented higher incidence of family history of cardiovascular disease (38.90% vs 25.94%), diabetes mellitus (34.87% vs 19.01%), impaired fasting glucose (21.91% vs 19.07%), target organ damage (29.1% vs 15.95%), and cardiovascular disease (27.09% vs 17.06%). Dyslipidaemia (52.90% vs 42.03%), fasting plasma glucose (116.10�38.9 vs 107.80�37.2), HbA1c (6.41�1.42 vs 5.96�0.94), serum creatinine (1.09�0.27 vs 1.03�0.24) and microalbuminuria (21.90% vs 10.95%) were significantly higher in RH. Predictors of RH, determined by a multivariate logistic regression analysis were left ventricular hypertrophy (OD 2.14, 95% CI 1.32-3.69), renal impairment expressed as eGFR [ 60 ml/min/1.73m2 (OD 1.62, 95% CI 1.21-2.21) and the presence of cardiovascular disease (OD 1.48, 95% CI 1.02-2.16).

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