Abstract P276: A High Sodium Diet Reduces Cutaneous Microvascular Function In Normotensive Individuals With Salt Sensitive Blood Pressure

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Jordan C Patik ◽  
Joseph M Stock ◽  
Nathan T Romberger ◽  
Shannon L Lennon ◽  
William B Farquhar ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Sodium Intake ◽  
Local Heating ◽  
Urinary Sodium Excretion ◽  
Microvascular Function ◽  
Dietary Sodium ◽  
Heating Unit ◽  
Doppler Flowmetry ◽  
High Sodium

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.

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 Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans

2019 ◽  
Vol 317 (1) ◽  
pp. H97-H103 ◽  
Author(s):  
Meghan G. Ramick ◽  
Michael S. Brian ◽  
Evan L. Matthews ◽  
Jordan C. Patik ◽  
Douglas R. Seals ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Vascular Function ◽  
Reactive Oxygen ◽  
Microvascular Function ◽  
High Salt ◽  
Dietary Sodium ◽  
Oxygen Species ◽  
High Sodium ◽  
Cutaneous Vasodilation

It has previously been shown that high dietary salt impairs vascular function independent of changes in blood pressure. Rodent studies suggest that NADPH-derived reactive oxygen species mediate the deleterious effect of high salt on the vasculature, and here we translate these findings to humans. Twenty-nine healthy adults (34 ± 2 yr) participated in a controlled feeding study. Participants completed 7 days of a low-sodium diet (LS; 20 mmol sodium/day) and 7 days of a high-sodium diet (HS; 300 mmol sodium/day) in random order. All participants were salt resistant, defined as a ≤5-mmHg change in 24-h mean BP determined while on the LS and HS diets. Laser Doppler flowmetry was used to assess cutaneous vasodilation in response to local heating (42°C) during local delivery of Ringer’s ( n = 29), 20 mM ascorbic acid (AA; n = 29), 10 µM Tempol ( n = 22), and 100 µM apocynin ( n = 22). Additionally, endothelial cells were obtained in a subset of participants from an antecubital vein and stained for nitrotyrosine ( n = 14). Cutaneous vasodilation was attenuated by the HS diet compared with LS [LS 93.0 ± 2.2 vs. HS 86.8 ± 2.0 percentage of maximal cutaneous vascular conductance (%CVCmax); P < 0.05] and was restored by AA during the HS diet (AA 90.7 ± 1.2 %CVCmax; P < 0.05 vs. HS). Cutaneous vasodilation was also restored with the local infusion of both apocynin ( P < 0.01) and Tempol ( P < 0.05) on the HS diet. Nitrotyrosine expression was increased on the HS diet compared with LS ( P < 0.05). These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. NEW & NOTEWORTHY High-sodium diets have deleterious effects on vascular function, likely mediating, in part, the increased cardiovascular risk associated with a high sodium intake. Local infusion of apocynin and Tempol improved microvascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt. This study provides insight into the blood pressure-independent mechanisms by which dietary sodium impairs vascular function. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/dietary-sodium-oxidative-stress-and-microvascular-function/ .

Abstract 54: Genome-Wide Association Analysis of Gene-Sodium Interactions on Blood Pressure Phenotypes: The GenSalt Study

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
Changwei Li ◽  
Jiang He ◽  
James Hixson ◽  
Dongfeng Gu ◽  
Dabeeru Rao ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Meta Analysis ◽  
Snp Array ◽  
Urinary Sodium Excretion ◽  
Dietary Sodium ◽  
Nucleotide Polymorphisms ◽  
Genome Wide ◽  
Inverse Variance ◽  
Meta Analyses

Background: Elevated blood pressure (BP) is a major public health challenge. Although the heritability of BP has been long established, current findings can explain only a small proportion of the BP variability attributed to genetic factors. Recent studies indicate that gene-environmental interactions may help to identify novel BP loci. Hence, the current study aimed to identify genetic variants influencing BP regulation by conducting genome-wide gene-sodium interaction analyses among 1,906 participants of the Genetic Epidemiology Network of Salt-Sensitivity (GenSalt) study. Methods: GenSalt recruited 1,906 Chinese participants from 633 families. At baseline, one 24-hour and two 8-hour urine specimens were collected to measure urinary sodium excretion. Nine BP measurements were taken using a random zero sphygmomanometer. A total of 868,158 autosomal single nucleotide polymorphisms (SNPs) were genotyped using Affymetrix Genomewide Human SNP array 6.0 (Affymetrix, Inc, Santa Clara, CA). Mixed effects models were used to test genome-wide SNP-sodium interactions on BP, adjusting for age, gender, and body mass index. Promising findings (interaction term P <1.00х10 -6 ) from GenSalt were further evaluated for replication among Chinese participants of the Multi-Ethnic Study of Atherosclerosis (MESA) with available data from the database of genotypes and phenotypes (dbGaP). SNP effects in GenSalt and MESA were meta-analyzed using inverse-variance weighted fixed effect models. Results: The meta-analyses identified 3 novel loci that significantly interacted with sodium to influence BP phenotypes. SNP-sodium interactions on systolic BP were identified for NEK2 variant rs10494938 at 1q32.3 (GenSalt P =2.19х10 -6 , MESA P =4.35х10 -4 , and Meta-analysis P = 3.93х10 -8 ). In addition, CASP4 variant rs1944900 at 11q22.3 interacted with sodium to influence both systolic BP (GenSalt P =1.24х10 -9 , MESA P =4.22х10 -2 , and Meta-analysis P = 1.14х10 -10 ) and mean arterial pressure (GenSalt P =1.68х10 -9 , MESA P =4.27х10 -2 , and Meta-analysis P = 1.91х10 -10 ). Furthermore, C9orf3 variant rs17679141 at 9q22.32 interacted with sodium to influence diastolic BP (GenSalt P =2.85х10 -8 , MESA P =4.55х10 -2 , and Meta-analysis P =4.61х10 -9 ). The 3 variants all physically mapped to the intronic regions of their corresponding genes. Conclusion: The current study identified 3 novel loci which may interact with dietary sodium intake to influence BP phenotypes.

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.

Dietary sodium and central vs. peripheral ouabain-like activity in Dahl salt-sensitive vs. salt-resistant rats

1994 ◽  
Vol 267 (5) ◽  
pp. H1916-H1920 ◽  
Author(s):  
F. H. Leenen ◽  
E. Harmsen ◽  
H. Yu
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
High Sodium ◽  
High Sodium Intake ◽  
Pressor Responses ◽  
Excess Sodium

To assess the possible contribution of brain ouabain-like activity (OLA) to the pressor effects of high-sodium intake in Dahl salt-sensitive (Dahl S) rats, we assessed the effects of high (8%) on blood pressure (BP) and peripheral and brain OLA in Dahl on blood pressure (BP) and peripheral and brain OLA in Dahl S and Dahl salt-resistant (Dahl R) rats. On regular sodium intake, Dahl S and R had similar BP; however, by 7 wk of age adrenal and plasma OLA were 15–30% higher in Dahl S vs. R, whereas central OLA remained similar. On high-sodium intake, in Dahl S both peripheral and central OLA increased within 1 wk with additional increases after 3 wk. These increases preceded the rise in BP. In Dahl R rats, high sodium did not increase BP. However, 3 wk of high sodium did increase peripheral as well as central OLA, the latter to a lesser extent compared with Dahl S and not in the hypothalamus. These results are consistent with the concept that central OLA may be involved in the pressor responses to high sodium in Dahl S. Circulating OLA may play a role in the regulation of renal function to excrete excess sodium in both strains.

Dietary Na and baroreflex modulation of blood pressure and RSNA in normotensive vs. spontaneously hypertensive rats

1994 ◽  
Vol 266 (2) ◽  
pp. H496-H502 ◽  
Author(s):  
B. S. Huang ◽  
F. H. Leenen
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Sodium Intake ◽  
Marked Change ◽  
Dietary Sodium ◽  
Hypertensive Rats ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
Wistar Kyoto

Different changes in baroreflex control of the circulation have been postulated to play a role in the different blood pressure (BP) effects of dietary sodium in normotensive vs. genetically hypertensive rats. We therefore evaluated in young Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR), with or without chronic sinoaortic denervation (SAD), the effects of low, regular, and high dietary sodium intake from 4 to 8 wk of age on BP and baroreflex function. The latter was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate in response to (de)pressor agents. In SHR, the above range of sodium caused a marked change in resting BP, somewhat more in intact (48 mmHg) vs. SAD (36 mmHg) rats. In contrast, in WKY this range of sodium intake caused only a minor (7 mmHg) change in resting BP of intact WKY but a significant (16 mmHg) change in WKY with SAD, mainly due to an increase in BP on high sodium. In intact WKY increasing dietary sodium from low to regular to high caused stepwise increases in the gain of the RSNA-BP reflex, whereas in intact SHR only an increase from low to regular sodium intake increased the gain. After SAD, the gain of the RSNA-BP reflex was very low, and no longer affected by dietary sodium in either strain. These data suggest that in WKY a sensitization in arterial baroreflex control of RSNA prevents a sodium-induced increase in BP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of dietary sodium on vasoconstriction and eNOS-mediated vascular relaxation in caveolin-1-deficient mice

2008 ◽  
Vol 294 (3) ◽  
pp. H1258-H1265 ◽  
Author(s):  
Luminita H. Pojoga ◽  
Tham M. Yao ◽  
Sumi Sinha ◽  
Reagan L. Ross ◽  
Jeffery C. Lin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Vascular Function ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Vascular Relaxation ◽  
Enos Expression ◽  
Vascular Contraction ◽  
Caveolin 1 ◽  
Enos Activity

Changes in dietary sodium intake are associated with changes in vascular volume and reactivity that may be mediated, in part, by alterations in endothelial nitric oxide synthase (eNOS) activity. Caveolin-1 (Cav-1), a transmembrane anchoring protein in the plasma membrane caveolae, binds eNOS and limits its translocation and activation. To test the hypothesis that endothelial Cav-1 participates in the dietary sodium-mediated effects on vascular function, we assessed vascular responses and nitric oxide (NO)-mediated mechanisms of vascular relaxation in Cav-1 knockout mice (Cav-1−/−) and wild-type control mice (WT; Cav-1+/+) placed on a high-salt (HS; 4% NaCl) or low-salt (LS; 0.08% NaCl) diet for 16 days. After the systolic blood pressure was measured, the thoracic aorta was isolated for measurement of vascular reactivity and NO production, and the heart was used for measurement of eNOS expression and/or activity. The blood pressure was elevated in HS mice treated with NG-nitro-l-arginine methyl ester and more so in Cav-1−/− than WT mice and was significantly reduced during the LS diet. Phenylephrine caused vascular contraction that was significantly reduced in Cav-1−/− (maximum 0.25 ± 0.06 g/mg) compared with WT (0.75 ± 0.22 g/mg) on the HS diet, and the differences were eliminated with the LS diet. Also, vascular contraction in response to membrane depolarization by high KCl (96 mM) was reduced in Cav-1−/− (0.27 ± 0.05 g/mg) compared with WT mice (0.53 ± 0.12 g/mg) on the HS diet, suggesting that the reduced vascular contraction is not limited to a particular receptor. Acetylcholine (10−5 M) caused aortic relaxation in WT mice on HS (23.6 ± 3.5%) and LS (23.7 ± 5.5%) that was enhanced in Cav-1−/− HS (72.6 ± 6.1%) and more so in Cav-1−/− LS mice (93.6 ± 3.5%). RT-PCR analysis indicated increased eNOS mRNA expression in the aorta and heart, and Western blots indicated increased total eNOS and phosphorylated eNOS in the heart of Cav-1−/− compared with WT mice on the HS diet, and the genotypic differences were less apparent during the LS diet. Thus Cav-1 deficiency during the HS diet is associated with decreased vasoconstriction, increased vascular relaxation, and increased eNOS expression and activity, and these effects are altered during the LS diet. The data support the hypothesis that endothelial Cav-1, likely through an effect on eNOS activity, plays a prominent role in the regulation of vascular function during substantial changes in dietary sodium intake.

Impact of high sodium intake on blood pressure and functional sympatholysis during rhythmic handgrip exercise

2020 ◽  
Vol 45 (6) ◽  
pp. 613-620
Author(s):  
Jacob T. Caldwell ◽  
Shelbi L. Sutterfield ◽  
Hunter K. Post ◽  
Garrett M. Lovoy ◽  
Heather R. Banister ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brachial Artery ◽  
Sodium Intake ◽  
Cardiovascular Responses ◽  
Dietary Sodium ◽  
Handgrip Exercise ◽  
High Sodium ◽  
High Sodium Intake ◽  
Healthy Humans ◽  
Functional Sympatholysis

High dietary sodium intake is a risk factor for arterial hypertension; given that the ability to overcome sympathetically mediated vasoconstriction (functional sympatholysis) is attenuated in individuals with hypertension, we investigated the cardiovascular responses to high salt (HS) intake in healthy humans. We hypothesized that a HS intake of 15 g/day for 7 days would attenuate functional sympatholysis and augment the blood pressure response to handgrip exercise (HGE). Thirteen participants (6 males, 7 females) underwent 2 individual days of testing. Beat-by-beat blood pressure and heart rate were recorded throughout the trial on the non-exercising limb. Forearm blood flow was derived from ultrasonography on the brachial artery of the exercising limb. Participants then underwent a flow-mediated dilation (FMD) test. Next, a submaximal HGE was performed for 7 min with lower body negative pressure initiated during minutes 5–7. A single spot urine sample revealed a significant increase in sodium excretion during the HS conditions (p < 0.01). FMD was reduced during the HS condition. Mean arterial pressure was significantly higher during HS intake. No alteration to functional sympatholysis was found between conditions (p > 0.05). In summary, HS intake increases blood pressure without impacting functional sympatholysis or blood pressure responsiveness during HGE. These findings indicate that brachial artery dysfunction precedes an inefficient functional sympatholysis. Novelty Functional sympatholysis was not impacted by 1 week of high sodium intake. High sodium intake augmented the rate pressure product during handgrip exercise in healthy humans.

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

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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