scholarly journals The role of caloric intake in the association of high salt intake with high blood pressure

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Naftali Stern ◽  
Assaf Buch ◽  
Rebecca Goldsmith ◽  
Lesley Nitsan ◽  
Miri Margaliot ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Substantial Reduction ◽  
Caloric Intake ◽  
Community Dwelling ◽  
Dietary Sodium ◽  
Cross Sectional Survey ◽  
High Salt Intake

AbstractSince current recommendations call for a substantial reduction in overall sodium consumption, we tested whether or not these recommendations are implemented in common large subpopulations such as those with abnormal weight or hypertension in the current high sodium, high-calorie nutritional environment. In a national representative cross-sectional survey of the community-dwelling subjects aged 25–65 years conducted in Israel between 2015 and 2017, 582 randomly selected subjects completed health and dietary questionnaires, underwent blood pressure and anthropometric measurements and collected 24-h urine specimens, to assess dietary sodium intake. Overall mean 24-h sodium excretion was 3834 mg, more than double the recommended upper intake for adults < 1500 mg/day. Sodium excretion was directly related to caloric intake and blood pressure and linked to the presence of hypertension and overweight/obesity. The highest sodium excretion was seen in overweight/obese hypertensive subjects. This recent national survey shows a high consumption of sodium in the Israeli population and a dose–response association between caloric intake and urinary sodium excretion, independent of BMI and hypertension. Nevertheless, overweight/obese subjects with hypertension consume (excrete) more sodium than other BMI/ blood pressure-related phenotypes and may thus comprise a target subpopulation for future efforts to reduce sodium intake.

scholarly journals High-Salt Diet Accelerated the Decline of Residual Renal Function in Patients With Peritoneal Dialysis

2021 ◽  
Vol 8 ◽  
Author(s):  
Nirong Gong ◽  
Chun Zhou ◽  
Jianxia Hu ◽  
Xiaohong Zhong ◽  
Zhixiu Yi ◽  
...  
Keyword(s):  
Renal Function ◽  
Peritoneal Dialysis ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Residual Renal Function ◽  
High Salt ◽  
Dietary Sodium ◽  
High Salt Intake

Objective: This study aims to investigate the relationship between dietary salt intake and residual renal function in peritoneal dialysis (PD) patients.Methods: The daily salt intake of the patients was calculated based on a 3 day dietary record. Sixty-two patients were divided into three groups: 33 patients in the low salt intake group (salt intake &lt;6.0 g/day), 17 in the medium salt intake group (salt intake 6.0 to &lt;8.0 g/day), and 12 in the high salt intake group (salt intake ≥8.0 g/day). Regular follow-up was conducted every 3 months. Urine volume, peritoneal ultrafiltration volume, and other clinical indicators were recorded. Biochemical indexes were detected to evaluate the changes in residual renal function and peritoneal function during follow-up.Results: A positive correlation between dietary sodium intake and sodium excretion was found. During 12-month follow-up, a decrease of residual renal function showed a significant difference among the three groups (p = 0.041) (15.3 ± 27.5 vs. 12.5 ± 11.5 vs. 32.9 ± 18.4 L/W/1.73 m2 in the low-, medium-, and high salt intake groups, respectively). Consistently, a higher decline of residual renal function (adjusted β, 20.37; 95% CI, 2.83, 37.91) was found in participants with high salt intake (salt intake ≥8 g/day) compared with those in non-high salt intake.Conclusion: Our study showed that the sodium excretion by peritoneal dialysis was positively correlated with dietary sodium intake in PD patients. The high salt intake diet (salt intake ≥8 g/day) may lead to a faster decline of residual renal function in PD patients.

Blood Pressure and Intra-Erythrocyte Sodium during Normal and High Salt Intake in Middle-Aged Men: Relationship to Family History of Hypertension, and Neurogenic and Hormonal Variables

1984 ◽  
Vol 66 (4) ◽  
pp. 427-433 ◽  
Author(s):  
Ottar Gudmundsson ◽  
Hans Herlitz ◽  
Olof Jonsson ◽  
Thomas Hedner ◽  
Ove Andersson ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Family History ◽  
Salt Intake ◽  
Sodium Intake ◽  
Positive Family History ◽  
Sodium Content ◽  
High Salt Intake ◽  
History Of ◽  
Family History Of Hypertension ◽  
Erythrocyte Sodium

1. During 4 weeks 37 normotensive 50-year-old men identified by screening in a random population sample were given 12 g of NaCl daily, in addition to their usual dietary sodium intake. Blood pressure, heart rate, weight, urinary excretion of sodium, potassium and catecholamines, plasma aldosterone and noradrenaline and intra-erythrocyte sodium content were determined on normal and increased salt intake. The subjects were divided into those with a positive family history of hypertension (n = 11) and those without such a history (n = 26). 2. Systolic blood pressure and weight increased significantly irrespective of a positive family history of hypertension. 3. On normal salt intake intra-erythrocyte sodium content was significantly higher in those with a positive family history of hypertension. During high salt intake intra-erythrocyte sodium content decreased significantly in that group and the difference between the hereditary subgroups was no longer significant. 4. In the whole group urinary excretion of noradrenaline, adrenaline and dopamine increased whereas plasma aldosterone decreased during the increased salt intake. 5. Thus, in contrast to some earlier studies performed in young subjects, our results indicate that moderately increased sodium intake acts as a pressor agent in normotensive middle-aged men whether there was a positive family history of hypertension or not. We confirm that men with positive family history of hypertension have an increased intra-erythrocyte sodium content, and that an increase in salt intake seems to increase overall sympathetic activity.

Abstract 142: A Fructose-but Not a Glucose-enriched Diet, Induces a Salt-dependent Increase in Blood Pressure and Enhances NKCC2 Phosphorylation in Normal Rats

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Keyona N King-Medina ◽  
Emily Henson ◽  
Pablo Ortiz
Keyword(s):  
Blood Pressure ◽  
Drinking Water ◽  
Salt Intake ◽  
Caloric Intake ◽  
High Salt ◽  
Human Consumption ◽  
Thick Ascending Limb ◽  
Sprague Dawley ◽  
High Fructose ◽  
High Salt Intake

Human consumption of fructose as a sweetener has increased in the past 30 years. High fructose intake has been implicated in the development of hypertension, diabetes, and obesity. In the US, the upper 10th percentile of the population consumes up to 40% of their caloric intake from added sugars, in which fructose represents half of these. Fructose metabolism is strikingly different from that of glucose. Yet, the effect of a fructose or glucose-enriched diet in salt handling by the kidney, affecting blood pressure, and its interaction with high salt intake has been poorly studied. In genetic models of salt-sensitive hypertension, the activity of the Na + /K + /2Cl - cotransporter (NKCC2) in the thick ascending limb (TAL) is abnormally enhanced. We hypothesized that chronic fructose in drinking water induces a salt-dependent increase in blood pressure and stimulates NKCC2 during high salt intake in normal rats. Sprague-Dawley rats were given 20% fructose or 20% glucose in drinking water for 1 week after which a high salt (HS) diet (4% Na + in chow) was started for 3 weeks. When we measured systolic blood pressure (SBP) by tail cuff plethysmography in fructose-fed and glucose-fed rats on a HS diet, only the fructose-fed rats had an increased SBP from 120±10 to 132±6 mmHg on day 7 of HS (p<0.01). SBP continued to increase up to 144±18 mmHg after 3 weeks (p<0.01 vs glucose). Fructose or glucose alone did not increase SBP after 4 weeks. We then repeated the protocol using radiotelemetry to monitor the blood pressure (BP). In rats fed fructose, by day 5 of HS the SBP increased by 12±3 mmHg (p<0.02) and SBP remained elevated for 3 weeks (delta: 10±2.5 mmHg, n=3). In rats fed glucose, a HS diet did not significantly change SBP for 3 weeks (n=5). Moreover, NKCC2 activity in the TAL is enhanced by phosphorylation at Thr96, 101. We found that NKCC2 phosphorylation was higher in rats fed fructose plus HS (p<0.02) but not in rats fed glucose plus HS for 3 weeks (HS: 100, fructose+HS: 250±40%, glucose+HS: 95±10%). Therefore, we conclude that a high fructose (but not a glucose) diet in normal rats induces a salt-dependent increase in BP independently from caloric intake. Thus, the increase in BP may in part be due to the stimulation of NKCC2 phosphorylation in the TAL by fructose.

scholarly journals Sodium Intake and Hypertension

Nutrients ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1970 ◽  
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.

scholarly journals Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake

2002 ◽  
Vol 283 (3) ◽  
pp. F447-F453 ◽  
Author(s):  
Amy J. Mangrum ◽  
R. Ariel Gomez ◽  
Victoria F. Norwood
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Wild Type ◽  
Compensatory Mechanisms ◽  
Wide Range ◽  
Blood Pressures ◽  
Pressure Natriuresis

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.

Blood pressure variability in relation to 24-hour urinary sodium excretion in high salt intake polish population

2015 ◽  
Vol 9 (4) ◽  
pp. e72
Author(s):  
Katarzyna Stolarz-Skrzypek ◽  
Adam Bednarski ◽  
Grzegorz Kiełbasa ◽  
Malgorzata Kloch-Badelek ◽  
Danuta Czarnecka
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Blood Pressure Variability ◽  
Salt Intake ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
High Salt ◽  
Polish Population ◽  
High Salt Intake

scholarly journals Dietary sodium intake in urban and rural Malawi, and directions for future interventions

2018 ◽  
Vol 108 (3) ◽  
pp. 587-593 ◽  
Author(s):  
Josephine E Prynn ◽  
Louis Banda ◽  
Alemayehu Amberbir ◽  
Alison J Price ◽  
Ndoliwe Kayuni ◽  
...  
Keyword(s):  
Rural Communities ◽  
Salt Intake ◽  
Sodium Intake ◽  
Urinary Sodium ◽  
Sub Saharan Africa ◽  
Dietary Sodium ◽  
Cross Sectional Survey ◽  
Cross Sectional ◽  
Spot Urine ◽  
Per Capita

ABSTRACT Background High dietary sodium intake is a major risk factor for hypertension. Data on population sodium intake are scanty in sub-Saharan Africa, despite a high hypertension prevalence in most countries. Objective We aimed to determine daily sodium intake in urban and rural communities in Malawi. Design In an observational cross-sectional survey, data were collected on estimated household-level per capita sodium intake, based on how long participants reported that a defined quantity of plain salt lasts in a household. In a subset of 2078 participants, 24-h urinary sodium was estimated from a morning spot urine sample. Results Of 29,074 participants, 52.8% of rural and 50.1% of urban individuals lived in households with an estimated per capita plain salt consumption >5 g/d. Of participants with urinary sodium data, 90.8% of rural and 95.9% of urban participants had estimated 24-h urinary sodium >2 g/d; there was no correlation between household per capita salt intake and estimated 24-h urinary sodium excretion. Younger adults were more likely to have high urinary sodium and to eat food prepared outside the home than were those over the age of 60 y. Households with a member with previously diagnosed hypertension had reduced odds (OR: 0.59; 95% CI: 0.51, 0.68) of per capita household plain salt intake >5 g/d, compared with those where hypertension was undiagnosed. Conclusions Sodium consumption exceeds the recommended amounts for most of the population in rural and urban Malawi. Population-level interventions for sodium intake reduction with a wide focus are needed, targeting both sources outside the home as well as home cooking. This trial was registered at clinicaltrials.gov as NCT03422185.

Renal denervation chronically lowers arterial pressure independent of dietary sodium intake in normal rats

2003 ◽  
Vol 284 (6) ◽  
pp. H2302-H2310 ◽  
Author(s):  
Frédéric Jacob ◽  
Pilar Ariza ◽  
John W. Osborn
Keyword(s):  
Arterial Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Recovery Period ◽  
Control Period ◽  
Dietary Sodium ◽  
Renal Nerves ◽  
Dietary Salt ◽  
Dietary Salt Intake ◽  
High Salt Intake

The present study was designed to test the hypothesis that renal nerves chronically modulate arterial pressure (AP) under basal conditions and during changes in dietary salt intake. To test this hypothesis, continuous telemetric recording of AP in intact (sham) and renal denervated (RDNX) Sprague-Dawley rats was performed and the effect of increasing and decreasing dietary salt intake on AP was determined. In protocol 1, 24-h AP, sodium, and water balances were measured in RDNX ( n = 11) and sham ( n = 9) rats during 5 days of normal (0.4% NaCl) and 10 days of high (4.0% NaCl) salt intake, followed by a 3-day recovery period (0.4% NaCl). Protocol 2 was similar with the exception that salt intake was decreased to 0.04% NaCl for 10 days after the 5-day period of normal salt (0.04% NaCl) intake (RDNX; n = 6, sham; n = 5). In protocol 1, AP was lower in RDNX (91 ± 1 mmHg) compared with sham (101 ± 2 mmHg) rats during the 5-day 0.4% NaCl control period. During the 10 days of high salt intake, AP increased <5 mmHg in both groups so that the difference between sham and RDNX rats remained constant. In protocol 2, AP was also lower in RDNX (93 ± 2 mmHg) compared with sham (105 ± 4 mmHg) rats during the 5-day 0.4% NaCl control period, and AP did not change in response to 10 days of a low-salt diet in either group. Overall, there were no between-group differences in sodium or water balance in either protocol. We conclude that renal nerves support basal levels of AP, irrespective of dietary sodium intake in normal rats.

Abstract 055: Systemic Effect of Renal 11β-HSD2 Deficiency on Blood Pressure Regulation

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Kohei Ueda ◽  
Mitsuhiro Nishimoto ◽  
Daigoro Hirohama ◽  
Nobuhiro Ayuzawa ◽  
Wakako Kawarazaki ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Nervous Activity ◽  
Subcutaneous Administration ◽  
Systemic Effect ◽  
Dietary Sodium ◽  
Sympathetic Nervous Activity ◽  
Membrane Expression ◽  
Corticosterone Concentration ◽  
High Salt Intake

Background: Renal mechanism of 11β-HSD2 deficiency for developing hypertension is to be evaluated because vascular mechanism associated with sympathetic nervous activity was prevailing in global Hsd11b2 knockout (KO) mice although brain-specific KO mice needed high salt intake to develop hypertension. We have demonstrated the importance of renal 11β-HSD2 deficiency on developing hypertension by using kidney-specific Hsd11b2 knockout ( Hsd11b2 Ksp-/- ; KS-KO) mice ( Hypertension , in press) and have continued the analysis of the systemic effect of renal 11β-HSD2 deficiency. Method: Blood pressure (BP) and heart rate (HR) was measured by using 24h telemetry. Amiloride (25 mg/L) and hydrochlorothiazide (HCTZ, 300 mg/L) were administered through drinking water. Pellet containing MR antagonist spironolactone (MRA; 50 mg/KgBW/day) was administered subcutaneously. Corticosterone concentration was determined by ELISA. Data are presented as mean±SE. Result: Systolic and diastolic BPs of KS-KO mice were significantly higher, although the HR was lower, than those of WT mice: SBP, 142.4±1.0 vs 122.4±0.8 mmHg; DBP, 103.9±0.8 vs 94.4±0.8 mmHg; HR, 492.5±2.7 vs 555.4±2.4 (n=7). Mean BP was decreased to the level of WT mice by reducing dietary sodium content from 0.3 % to 0.01 %. Plasma [K + ] was significantly lower in KS-KO mice: 2.9±0.2 vs 4.2±0.2 mEq/L (n=5). Renal membrane expressions of NCC, T53-phosphorylated NCC (pNCC), cleaved ENaCα and full-length ENaCα were upregulated in KS-KO mice. Correction of plasma [K + ] of KS-KO mice by using high KCl diet or amiloride downregulated the renal membrane expression of pNCC and decreased the MBP to the level of WT mice as well as chronic HCTZ-treated KS-KO mice. Subcutaneous administration of MRA decreased MBP of KS-KO mice and the renal membrane expressions of pNCC and cleaved ENaCα. Diurnal variation of plasma corticosterone concentration was diminished in KS-KO mice and the urinary excretion of corticosterone was higher compared to that in WT mice. Conclusion: Renal 11β-HSD2 deficiency is sufficient in developing hypertension via MR activation induced by excessive corticosterone, the systemic effect of which are also suggested.

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

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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