Abstract P614: Relationship Of Sodium Intake And Stress With Bone Health In Women

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Allison Jasti ◽  
Deborah L Stewart ◽  
Gregory A Harshfield
Keyword(s):  
Bone Health ◽  
Salt Intake ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
African American Adolescents ◽  
Ang Ii ◽  
Mineral Density ◽  
High Sodium ◽  
Low Sodium ◽  
Relationship Of

Background: The skeleton is vital to sodium homeostasis, accounting for 40% of the body’s sodium. Research indicates stress and low sodium intake are independently associated with RAAS activation. In certain populations, stress can induce salt sensitivity, increasing the risk of hypertension and target organ damage, but the association of low versus high sodium intake with bone health is controversial. Purpose: This study sought out the relationship of low sodium and stress-induced RAAS activation with bone health. The tested hypothesis was those with lowest sodium intake would have lower total bone mineral density (TBMD) and content (TBMC) associated with stress-induced increases in angiotensin ii (Ang II) and aldosterone (Aldo). Methods: We compared effect of stress on Ang II, Aldo, TBMD and TMBC in healthy Caucasian and African-American adolescents. Subjects were grouped by quartiles based on sodium intake, assessed by urinary sodium excretion. Results: Due to females, overall significant inverse associations are observed between TBMD, TBMC, Ang II and Aldo in the lowest sodium intake quartile. Post-stress, women in the lowest sodium intake quartile showed that increases in both Ang II and Aldo correspond with lower TMBC and TMBD. There was no significance between Ang II, Aldo, TMBC and TMBD in the three highest quartiles of women nor in any male quartile. Conclusion: These data suggest Ang II and Aldo may reduce TMBC and TMBD in women. Stress-induced increases in Ang II and Aldo, with low sodium intake, may further reduce TBMD and TBMC in women. Ang II inhibition and/or moderated salt intake may be an efficacious prevention or treatment against the development of osteoporosis.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

Role of ETA receptors in experimental ANG II-induced hypertension in rats

2001 ◽  
Vol 281 (1) ◽  
pp. R150-R154 ◽  
Author(s):  
Jennifer R. Ballew ◽  
Gregory D. Fink
Keyword(s):  
Mean Arterial Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Male Rats ◽  
Ang Ii ◽  
High Sodium ◽  
High Sodium Intake ◽  
Induced Hypertension ◽  
Baseline Levels

The objectives were to determine if ANG II-induced hypertension is maintained by activation of endothelin type A (ETA) receptors by endogenous ET-1 and if this effect is influenced by salt intake. Male rats were maintained on high sodium intake (HS; 6 meq/day) or on normal sodium intake (NS; 2 meq/day). Hypertension was produced by intravenous infusion of ANG II (5 ng/min) for 15 days. Five-day oral dosing with the selective ETA-receptor antagonist ABT-627 (∼2 mg · kg−1 · day−1) reduced mean arterial pressure (MAP) to baseline levels in rats on HS receiving ANG II infusion, but it did not affect MAP in normotensive HS controls. In rats on NS, ABT-627 only transiently decreased MAP in rats receiving ANG II and slightly reduced MAP in normotensive controls. ABT-627 produced mild retention of sodium and water in NS rats receiving ANG II, but not in any other group. These results indicate that ET-1 plays a role in ANG II-induced hypertension via activation of ETAreceptors and that this role is more prominent in rats on HS.

scholarly journals Sodium Content of Foods Sold in the Spanish Market. Results from the BADALI Project

Nutrients ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 3410
Author(s):  
Marta Beltrá ◽  
Fernando Borrás ◽  
Ana B. Ropero
Keyword(s):  
Sodium Salt ◽  
Salt Intake ◽  
Sodium Intake ◽  
Salt Content ◽  
Daily Intake ◽  
Food Group ◽  
Sodium Content ◽  
High Sodium ◽  
Low Sodium ◽  
Pan American

High sodium/salt intake is a risk factor for Non-Communicable Diseases (NCDs). Excess sodium intake has been associated with high coronary heart disease, stroke and high blood pressure. The sodium daily intake is above the recommendations in the world as well as in Spain. Reducing salt content in processed foods and ready meals is one of the main strategies for reducing sodium intake. The aim of the present work is to characterise the presence of sodium in foods sold in the Spanish market. We also study a possible shift in sodium content in products over the last few years. For this purpose, 3897 products included in the BADALI food database were analysed, classified into 16 groups (G). We found that 93.3% of all foods displayed the sodium/salt content in the nutrition declaration. Meat—processed and derivatives (G8) had the highest mean and median values for sodium content, followed by snacks (G15) and sauces (G14). Only 12.7% of foods were sodium-free (≤ 5 mg/100 g or 100 mL), 32.4% had very low sodium (≤ 40 mg/100 g or 100 mL) and 48.2% were low in sodium (≤ 120 mg/100 g or 100 mL). On the contrary, 47.2% were high in sodium according to the Pan American Health Organisation Nutrient Profile Model (PAHO-NPM), while there were 31.9% according to the Chile-NPM. The agreement between the two NPMs was considered ‘substantial’ (κ = 0.67). When sodium content was compared over the years, no decrease was observed. This analysis was performed in the entire food population, by food group and in matched products. Therefore, more effort should be made by all parties involved in order to decrease the sodium/salt intake in the population.

ANG II chronically supports renal and lumbar sympathetic activity in sodium-deprived, conscious rats

1996 ◽  
Vol 271 (6) ◽  
pp. H2591-H2598 ◽  
Author(s):  
L. Xu ◽  
V. L. Brooks
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sodium Intake ◽  
Ang Ii ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
High Sodium ◽  
Low Sodium ◽  
Two Phases ◽  
Phenylephrine Infusion

The hypothesis that chronic elevations in endogenous angiotensin II (ANG II) increase sympathetic outflow in conscious, normotensive rats was tested by determining if acute blockade of ANG II receptors with losartan (10 mg/kg iv) decreases renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA), or heart rate (HR) more in rats with higher ANG II levels due to a low sodium (LS) diet compared with a control sodium (CS) or high sodium (HS) diet. In LS rats, losartan decreased (P < 0.05) mean arterial pressure (MAP) in two phases: an immediate decrease of 23 +/- 2 mmHg and a slower fall to 35 +/- 4 mmHg below control 40 min postlosartan. Five minutes after losartan, RSNA (149 +/- 13%), LSNA (143 +/- 5%), and HR (109 +/- 2%) were increased (P < 0.05). Despite further falls in MAP, the elevation in RSNA and HR remained constant, and LSNA decreased toward control (119 +/- 4%). After restoration of MAP to basal levels with methoxamine or phenylephrine infusion, RSNA (46 +/- 8%), LSNA (49 +/- 11%), and HR (76 +/- 2%) were suppressed (P < 0.05). In CS rats, losartan also initially decreased (P < 0.05) MAP by 6 +/- 2 mmHg and increased (P < 0.05) RSNA to 129 +/- 13%. When MAP was returned to control, RSNA was decreased (70 +/- 8%; P < 0.05) but less than in LS rats. In contrast, no changes in MAP, RSNA, LSNA, or HR were observed after losartan in HS rats. In conclusion, endogenous ANG II chronically supports RSNA, LSNA, and HR in conscious, normotensive low and normal sodium intake rats.

Plasma Angiotensin II Concentration Regulates Vascular but Not Adrenal Responsiveness to Restriction of Sodium Intake in Normal Man

1981 ◽  
Vol 61 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Bess F. Dawson-Hughes ◽  
T. J. Moore ◽  
R. G. Dluhy ◽  
N. K. Hollenberg ◽  
G. H. Williams
Keyword(s):  
Sodium Intake ◽  
Regression Line ◽  
Sodium Balance ◽  
Ang Ii ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Intake ◽  
Low Sodium ◽  
Vascular Responsiveness ◽  
High Sodium Diet

1. Sodium restriction increases adrenal and decreases vascular sensitivity to angiotensin II (ANG II). These responses may be mediated either by the circulating level of ANG II or other mechanisms also modified by a change in sodium balance. To assess the importance of the ANG II level, captopril, an oral converting enzyme inhibitor, was used to lower the plasma ANG II level to the sodium-loaded range while maintaining subjects in low sodium balance. 2. Normal volunteer subjects received an infusion of ANG II in increasing doses in three states: high sodium intake, low sodium intake and low sodium intake after pretreatment with captopril. 3. Basal levels of ANG II on high-sodium diet and low-sodium diet plus captopril were similar. In the ANG II infusion studies the slope of the aldosterone—ANG II regression line on low sodium intake was significantly steeper than that on high sodium intake. After the addition of captopril the slope was not decreased, indicating that the endogenous ANG II concentration is not necessary to maintain adrenal sensitivity during sodium restriction. 4. In the ANG II infusion studies the slope of the mean blood pressure—ANG II regression line on high sodium intake was significantly steeper than that on low sodium intake. The addition of captopril to sodium-restricted subjects caused the slope of the regression relationship to increase significantly, consistent with an enhanced vascular responsiveness when endogenous ANG II levels were lowered. However, the slope on low sodium plus captopril did not increase to the level of subjects on a high-sodium diet, suggesting that factors in addition to the circulating ANG II level are also important in regulating the vascular responsiveness to ANG II.

scholarly journals Role of the renin-angiotensin system during alterations of sodium intake in conscious mice

2001 ◽  
Vol 281 (3) ◽  
pp. R987-R993 ◽  
Author(s):  
Brian C. Cholewa ◽  
David L. Mattson
Keyword(s):  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sodium Level ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Ang Ii ◽  
Plasma Renin Concentration ◽  
Renin Angiotensin ◽  
High Sodium ◽  
Low Sodium

The present studies were performed to quantify circulating components of the renin-angiotensin-aldosterone axis and to determine the functional importance of this system during alterations in sodium intake in conscious mice. Increasing sodium intake from ∼200 to 1,000 μeq/day significantly decreased plasma renin concentration from 472 ± 96 to 304 ± 83 ng ANG I · ml−1 · h−1( n = 5) but did not alter plasma renin activity from the low-sodium level of 7.7 ± 1.1 ng ANG I · ml−1 · h−1. Despite the elevated plasma renin concentration, plasma ANG II in mice on low-sodium level averaged 14 ± 3 pg/ml and was significantly suppressed to 6 ± 1 pg/ml by high-sodium intake ( n = 7). Consistent with the modulation of ANG II, plasma aldosterone significantly decreased from 41 ± 8 to 8 ± 3 ng/dl when sodium intake was elevated ( n = 6). In a final set of experiments, the continuous infusion of ANG II (20 ng · kg−1 · min−1) led to a mild salt-sensitive increase in mean arterial pressure from 108 ± 2 to 131 ± 2 mmHg as sodium intake was varied from low to high ( n = 7). In vehicle-infused mice, mean arterial pressure was unaltered from 109 ± 2 mmHg when sodium intake was increased ( n = 6). These studies indicate that the physiological suppression of circulating ANG II may be required to maintain a constancy of arterial pressure during alterations in sodium intake in normal mice.

scholarly journals Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

Reproduction ◽  
2006 ◽  
Vol 131 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Jean St-Louis ◽  
Benoît Sicotte ◽  
Annie Beauséjour ◽  
Michèle Brochu
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Sodium ◽  
Sodium Diet ◽  
Uterine Arteries ◽  
Low Sodium Diet ◽  
Low Sodium

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

scholarly journals High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT2R-MasR axis in obese Zucker rats

2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain
Keyword(s):  
Sodium Intake ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Complex Nature ◽  
Ang Ii ◽  
Pronounced Increase ◽  
High Sodium ◽  
High Sodium Intake ◽  
Obese Rats ◽  
Obese Zucker Rats

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

Increased Renal Sensitivity to Aldosterone in the Potassium-Loaded Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 315s-317s
Author(s):  
W. R. Adam ◽  
J. W. Funder
Keyword(s):  
Sodium Intake ◽  
Control Diet ◽  
High Potassium ◽  
High Sodium ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High K ◽  
And Control

1. The renal response to aldosterone (urinary sodium and potassium excretion) was determined in adrenalectomized rats previously fed either a high potassium diet or a control diet. High K+ rats showed an enhanced response to aldosterone at all doses tested. 2. This enhanced response to aldosterone required the presence of the adrenal glands during the induction period, could be suppressed by a high sodium intake, but could not be induced by a low sodium diet. 3. No difference between high K+ and control rats could be detected in renal mineralocorticoid receptors, assessed by both in vivo and in vitro binding of tritiated aldosterone. 4. The method of the induction, and the mechanism of the enhanced response, remain to be defined.

scholarly journals Urine Spot Samples Can Be Used to Estimate 24-Hour Urinary Sodium Excretion in Children

2018 ◽  
Vol 148 (12) ◽  
pp. 1946-1953 ◽  
Author(s):  
Magali Rios-Leyvraz ◽  
Pascal Bovet ◽  
René Tabin ◽  
Bernard Genin ◽  
Michel Russo ◽  
...  
Keyword(s):  
Sodium Excretion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Population Level ◽  
Urinary Sodium Excretion ◽  
Cross Sectional Study ◽  
Urinary Sodium ◽  
Cross Sectional ◽  
High Sodium ◽  
Individual Level

ABSTRACT Background The gold standard to assess salt intake is 24-h urine collections. Use of a urine spot sample can be a simpler alternative, especially when the goal is to assess sodium intake at the population level. Several equations to estimate 24-h urinary sodium excretion from urine spot samples have been tested in adults, but not in children. Objective The objective of this study was to assess the ability of several equations and urine spot samples to estimate 24-h urinary sodium excretion in children. Methods A cross-sectional study of children between 6 and 16 y of age was conducted. Each child collected one 24-h urine sample and 3 timed urine spot samples, i.e., evening (last void before going to bed), overnight (first void in the morning), and morning (second void in the morning). Eight equations (i.e., Kawasaki, Tanaka, Remer, Mage, Brown with and without potassium, Toft, and Meng) were used to estimate 24-h urinary sodium excretion. The estimates from the different spot samples and equations were compared with the measured excretion through the use of several statistics. Results Among the 101 children recruited, 86 had a complete 24-h urine collection and were included in the analysis (mean age: 10.5 y). The mean measured 24-h urinary sodium excretion was 2.5 g (range: 0.8–6.4 g). The different spot samples and equations provided highly heterogeneous estimates of the 24-h urinary sodium excretion. The overnight spot samples with the Tanaka and Brown equations provided the most accurate estimates (mean bias: −0.20 to −0.12 g; correlation: 0.48–0.53; precision: 69.7–76.5%; sensitivity: 76.9–81.6%; specificity: 66.7%; and misclassification: 23.0–27.7%). The other equations, irrespective of the timing of the spot, provided less accurate estimates. Conclusions Urine spot samples, with selected equations, might provide accurate estimates of the 24-h sodium excretion in children at a population level. At an individual level, they could be used to identify children with high sodium excretion. This study was registered at clinicaltrials.gov as NCT02900261.

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