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Cited by 40Sodium Intake and HealthRenin-Angiotensin System StudiesBlood Pressure and Hypertension Studies

Reducing Dietary Sodium to 1000 mg per Day Reduces Neurovascular Transduction Without Stimulating Sympathetic Outflow

Open access
Babcock, Matthew C., Robinson, Austin T., Migdal, Kamila U., Watso, Joseph C., Wenner, Megan M., Stocker, Sean D., Farquhar, William B.·2019·Hypertension
DOI 10.1161/hypertensionaha.118.12074PMC PMC6374182
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Abstract

The American Heart Association recommends no more than 1500 mg of sodium/day as ideal. Some cohort studies suggest low-sodium intake is associated with increased cardiovascular mortality. Extremely low-sodium diets (≤500 mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow. The effects of an American Heart Association–recommended diet on sympathetic regulation of the vasculature are unclear. Therefore, we assessed whether a 1000 mg/d diet alters sympathetic outflow and sympathetic vascular transduction compared with the more commonly recommended 2300 mg/d. We hypothesized that sodium reduction from 2300 to 1000 mg/d would not affect resting sympathetic outflow but would reduce sympathetic transduction in healthy young adults. Seventeen participants (age: 26±2 years, 9F/8M) completed 10-day 2300 and 1000 mg/d sodium diets in this randomized controlled feeding study (crossover). We measured resting renin activity, angiotensin II, aldosterone, blood pressure, muscle sympathetic nerve activity, and norepinephrine. We quantified beat-by-beat changes in mean arterial pressure and leg vascular conductance (femoral artery ultrasound) following spontaneous sympathetic bursts to assess sympathetic vascular transduction. Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone ( P <0.01 for all) but did not alter mean arterial pressure (78±2 versus 77±2 mm Hg, P =0.56), muscle sympathetic nerve activity (13.9±1.3 versus 13.9±0.8 bursts/min, P =0.98), or plasma/urine norepinephrine. Sympathetic vascular transduction decreased ( P <0.01). These data suggest that reducing sodium from 2300 to 1000 mg/d stimulates the renin-angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults.

Integrity signals

Registry

Crossref · 10.1161/hypertensionaha.118.12074

Cites

43 of 43 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

31 of 40 cited sources checked · 12 supported · 0 flagged · accuracy not yet measured

  • Premisecitation

    Lower dietary sodium has been shown to enhance endothelial function.

    “Reduced dietary sodium has been shown to improve endothelial function,13, 17, 18, 21”
    Quote in the paperSubstantial claim4 of 4 sources checked
  • Premisecitation

    In normotensive people at elevated risk of future hypertension, each MSNA burst has been reported to cause larger drops in vascular conductance and rises in blood pressure.

    “Greater declines in vascular conductance and increases in BP with each burst of MSNA (i.e., neurovascular transduction) have recently been reported in normotensive individuals who are at heightened risk for future development of hypertension,20”
    Quote in the paperSubstantial claim1 of 1 sources checked
  • Premisecitation

    Few people voluntarily consume a diet as low as 500 mg sodium per day.

    “it is rare for anyone to voluntarily follow a diet that low in sodium,19”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [19] source

      The Discussion (page not specified) reports mean 24-hour sodium excretion of about 3,526 mg, well above the 500 mg/day level in the claim. That supports the point that typical intake is much higher, but the paper does not establish how rarely individuals voluntarily follow a 500 mg/day diet. (LLM, conf=0.78)

      Experimental — accuracy not yet measured
  • Premisecitation

    Sodium intake and RAAS activation are strongly inversely related.

    “Due to the robust inverse relation between sodium intake and RAAS activation,7, 17, 18”
    Quote in the paperSubstantial claim3 of 3 sources checked
    • cites [7] source

      The ‘Effect on hormones and lipids’ section reports that modest salt reduction produced a small increase in plasma renin activity and aldosterone, supporting an inverse direction of effect. It does not establish a robust inverse relation across sodium intakes; the hormone measurements came from trials lasting only four to six weeks, and the authors say the effects might attenuate over time. (LLM, conf=0.87)

      Experimental — accuracy not yet measured
    • cites [17] source
    • cites [18] source
  • Premisecitation

    The RAAS values on the 1000 mg/day diet were within normal physiological ranges previously reported.

    “the values we present here are within normal physiological values previously reported in the literature 34”
    Quote in the paperNot a substantial claim1 of 1 sources checked
  • May combine two claims. 16
  • Classified as probably not a substantial claim. 20

  • May combine two claims.

    Premisecitation

    Diets with sodium at or below 500 mg per day activate the renin-angiotensin-aldosterone system and raise sympathetic outflow.

    “Extremely low sodium diets (≤500mg/d) elicit activation of the renin-angiotensin-aldosterone system and stimulate sympathetic outflow.”
    • Also stated in: § Introduction · boosted
      “Experimental studies using extremely low sodium diets (≤500mg/d) increase muscle sympathetic nerve activity (MSNA)14–16 and elicit a robust activation of the renin angiotensin aldosterone system (RAAS).7, 17, 18”
    Quote in the paperSubstantial claim3 of 6 sources checked
    • cites [14] source
    • cites [15] source
    • cites [16] source
    • cites [7] source

      The ‘Effect on hormones and lipids’ section says salt reduction stimulates the renin-angiotensin-aldosterone and sympathetic systems, particularly after sudden, large reductions. It does not establish a threshold of ≤500 mg of sodium per day; its own meta-analysis concerns longer-term modest salt reduction and reports only small physiological increases. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [17] source

      The Methods describe a low-sodium diet of 20 mmol/day (about 460 mg/day), and the Results report higher plasma renin activity and serum aldosterone on that diet than on the high-sodium diet. This supports the renin–aldosterone portion for the studied adults, but the paper does not report increased sympathetic outflow or establish the claim for all diets at or below 500 mg/day. (LLM, conf=0.86)

      Experimental — accuracy not yet measured
    • cites [18] source

      The Methods describe a low-sodium diet of 20 mmol/day (about 460 mg/day), and the Results show higher renin activity, angiotensin II, and aldosterone on that diet than on the high-sodium diet. The paper does not report sympathetic outflow, so it does not support that part of the claim. Page numbers are unavailable in our copy. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim.

    Premisecitation

    The American Heart Association's ideal sodium intake recommendation is no more than 1500 mg per day.

    “The American Heart Association recommends no more than 1500mg of sodium/day as ideal.”
    • Also stated in: § Introduction · plain
      “the American Heart Association (AHA) recommends no more than 1500mg/d of sodium as ideal for CV health.3–7”
    Quote in the paperSubstantial claim4 of 5 sources checked
    • cites [3] source
    • cites [4] source

      The Introduction discusses international salt-intake recommendations, and the Implications section identifies a WHO target of 5 g of salt per day. Searches for the American Heart Association and a 1500 mg/day sodium limit found no passage in our copy stating the claimed recommendation; the WHO target does not establish what the AHA recommends. (LLM, conf=0.76)

      Experimental — accuracy not yet measured
    • cites [5] source
    • cites [6] source

      The Introduction discusses an Institute of Medicine assessment of sodium intake below 2,300 mg/day, and the Discussion mentions an Institute of Medicine recommendation for gradual sodium reduction. Neither passage states the American Heart Association’s ideal intake recommendation. Searches for the American Heart Association and a 1,500 mg/day limit found no passage in our copy establishing the claim. (LLM, conf=0.72)

      Experimental — accuracy not yet measured
    • cites [7] source

      The Dose-response to salt reduction section reports a US recommendation of 1.5 g (1500 mg) sodium per day, but only for about half the population; it gives a limit of less than 2.3 g/day for most adults. The passage does not identify the American Heart Association as the source or describe 1500 mg/day as its ideal recommendation. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • Classified as probably not a substantial claim.

    Study design and conductcitation

    The spike-triggered averaging methods have been shown to reliably quantify changes in blood pressure and blood flow caused by MSNA bursts.

    “These methods have been shown to reliably quantify changes in BP and blood flow induced by bursts of MSNA.26, 27”
    Quote in the paperSubstantial claim2 of 2 sources checked
    • cites [26] source

      The Methods and Results (pages unavailable) show that spike-triggered averaging quantified changes in mean arterial pressure and leg vascular conductance following MSNA bursts, with no systematic changes in the white-noise control. The paper measured femoral blood flow to calculate conductance, but it does not report burst-triggered changes in blood flow itself or directly test the method’s reliability. (LLM, conf=0.83)

      Experimental — accuracy not yet measured
    • cites [27] source

      The Methods describe spike-triggered averaging of mean arterial pressure and forearm vascular conductance after MSNA bursts. The Results report changes in both, while the Discussion says a white-noise control supports the method’s specificity. The paper reports burst-triggered conductance, however, rather than directly quantifying burst-triggered blood flow. (LLM, conf=0.82)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    The 2013 AHA/American College of Cardiology guidelines concluded that lowering habitual sodium to 2400 mg/day reduces blood pressure, and lowering further to 1500 mg/day reduces it more.

    “In the 2013 joint AHA/American College of Cardiology guidelines on lifestyle management to CV risk, it was concluded that reducing habitual sodium to 2,400mg/d results in BP reduction, and a further sodium reduction to 1500mg/d results in an even greater reduction in BP.41”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Racial differences in neurovascular transduction appear to contribute to exaggerated blood pressure variability in African American males, who are at higher risk of future hypertension.

    “Importantly the racial differences in neurovascular transduction appear to contribute to exaggerated BP variability in African American males, a group at heightened risk for future incidence of hypertension.20”
    Quote in the paperNot a substantial claim1 of 1 sources checked

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Sympathetic vascular transduction is likely affected by circulating vasoconstrictors and vasodilators such as endothelin-1 and nitric oxide.

    “In addition, sympathetic vascular transduction is likely influenced by circulating vasoconstrictors and vasodilators such as endothlin-138 and nitric oxide.39”
    Quote in the paperNot a substantial claim2 of 2 sources checked
    • cites [38] source

      The Perspectives (p. 9) report that endothelin-A signaling constrains blood flow during exercise in older adults, supporting endothelin-1’s role in vascular tone. The paper does not establish that endothelin-1 alters sympathetic vascular transduction specifically. Nitric oxide has a separate citation in the citing sentence and is not assessed here. (LLM, conf=0.82)

      Experimental — accuracy not yet measured
    • cites [39] source

      The Results and Discussion show that nitric oxide contributes to vasodilation in the superficial femoral artery after a brief ischemic stimulus. The paper does not examine whether nitric oxide influences sympathetic vascular transduction, which is the specific relationship attributed to it here. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    High sodium intake does not increase urine volume.

    “in accordance with recent findings indicating that high sodium intake does not increase urine volume.32”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [32] source

      The Figure 1 results report that a 6-g/day increase in salt intake did not significantly increase urine volume. The unqualified claim is stronger than that finding: the Discussion (p. 1938) notes divergent results in other studies, and the paper reports some diuresis with increased urinary salt excretion. (LLM, conf=0.85)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Premisecitation

    The authors previously found even higher RAAS levels with a 500 mg/day sodium diet without short-term adverse effects.

    “we have previously shown even greater RAAS levels using a 500 mg/d sodium diets with no short-term adverse effects.18”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [18] source

      The Methods (page unavailable) describe a seven-day low-sodium diet of 20 mmol/day, approximately 460 mg/day. The Results (page unavailable) report higher renin activity, angiotensin II, and aldosterone on that diet than on the high-sodium diet, with no difference in measured blood pressure. The paper does not establish the broader claim that the low-sodium diet had no short-term adverse effects. (LLM, conf=0.83)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Neurovascular transduction is mediated by α-adrenergic receptors.

    “This work has established that neurovascular transduction is mediated by α-adrenergic receptors,27”
    Quote in the paperNot a substantial claim1 of 1 sources checked
    • cites [27] source

      The Abstract reports that α-adrenergic blockade eliminated the forearm vasoconstriction following sympathetic bursts in young men at rest. But the Discussion says the initial increase in forearm vascular conductance was unchanged by blockade. The source therefore supports α-adrenergic mediation of the vasoconstrictor component, not neurovascular transduction without qualification. (LLM, conf=0.84)

      Experimental — accuracy not yet measured

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Reduced sodium diets improve endothelial function and nitric oxide bioavailability.

    “We have previously demonstrated that reduced sodium diets result in improved endothelial function and nitric oxide bioavailability.13, 17, 21, 40”
    Quote in the paperNot a substantial claim4 of 4 sources checked
    • cites [13] source

      The ARTERIES section (page unavailable) reports that sodium restriction improved endothelial function in adults with elevated blood pressure. It also says high sodium likely reduces nitric oxide bioavailability, but does not establish that a reduced-sodium diet improves nitric oxide bioavailability. (LLM, conf=0.84)

      Experimental — accuracy not yet measured
    • cites [17] source

      The Results (page not provided) report higher brachial artery flow-mediated dilation during the low-sodium diet than during the high-sodium diet, supporting improved endothelial function. The Discussion (page not provided) explicitly says the study did not assess altered nitric oxide bioavailability, so it does not establish that the reduced-sodium diet improved it. (LLM, conf=0.91)

      Experimental — accuracy not yet measured
    • cites [21] source

      The Results (Vascular Function; page unavailable) report higher flow-mediated dilation on the low-sodium diet than on the high-sodium diet, supporting the endothelial-function part of the claim. The Discussion (page unavailable) says the mechanism is unknown and discusses nitric oxide only as a possible explanation; it does not report improved nitric oxide bioavailability. (LLM, conf=0.88)

      Experimental — accuracy not yet measured
    • cites [40] source

      The Microvascular function results report better cutaneous vasodilation on the low-sodium than the high-sodium diet in normotensive adults with salt-resistant blood pressure. However, the difference in nitric oxide’s contribution between diets did not reach statistical significance (P = 0.075), and nitric oxide bioavailability was not directly measured. The claim therefore overstates that part of the finding and generalizes beyond the microvascular response studied. (LLM, conf=0.86)

      Experimental — accuracy not yet measured

  • May combine two claims.

    Findingnone given

    Serum sodium and urinary sodium excretion were lower on the 1000 mg/day diet than on the 2300 mg/day diet.

    “Serum sodium and urinary sodium excretion were lower on the 1000mg/d diet compared to the 2300mg/d diet (Table 2).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    The 1000 mg/day sodium diet did not change plasma or urinary norepinephrine compared with the 2300 mg/day diet.

    “or plasma/urine norepinephrine.”
    • Also stated in: § Results · plain
      “plasma NE was not different on the 1000mg/d sodium diet compared to the 2300mg/d sodium diet (Figure 2E). Urinary NE excretion was also not different on the 1000mg/day sodium diet compared to the 2300mg/d sodium diet (30.6±3.3 vs. 23.5±3.1ng/min, p>0.10).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    The 1000 mg/day sodium diet raised plasma renin activity, angiotensin II, and aldosterone relative to the 2300 mg/day diet.

    “Reducing sodium to 1000 mg/d increased renin activity, angiotensin II, and aldosterone (p<0.01 for all)”
    • Also stated in: § Results · plain
      “PRA (Figure 1A), circulating Aldo (Figure 1B), and Ang-II (Figure 1C) were elevated on the 1000mg/d diet compared to the 2300mg/d sodium diet.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Findingown data

    Urine volume was similar between the two diets.

    “Urine volume was also similar between diets”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    In a subset, changes in angiotensin II correlated with changes in transduction measured by MAP (r=0.84, p=0.01) and by leg vascular conductance (r=-0.80, p=0.03).

    “Changes in Ang II were significantly related to the change in transduction measured via MAP (n=8, Pearson’s r=0.84, p=0.01) and LVC (n=7, Pearson’s r=−0.80, p=0.03).”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Premisecitation

    Renal sodium excretion and RAAS hormones are inversely related, with higher RAAS activity causing greater sodium reabsorption.

    “The RAAS hormones are inversely related to sodium excretion by the kidneys, whereby elevated RAAS activity results in greater sodium reabsorption.33”
    Quote in the paperNot a substantial claim0 of 1 sources checked
    • cites [33]

      Couldn’t be matched to a paper in Crossref, so it can’t be checked.

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    The two diets were isocaloric and matched for potassium at 2500 mg/day.

    “The diets were 10 days each, isocaloric, matched for potassium (2500mg/d), and given in a randomized order separated by a ≥four-week washout.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    The study did not control for menstrual status in female participants.

    “we did not control for menstrual status in female participants.”
    Quote in the paperNot a substantial claim

  • Classified as probably not a substantial claim.

    Study design and conductnone given

    Sympathetic neurograms were visually inspected by a blinded lab member trained in MSNA analysis.

    “Sympathetic neurograms were analyzed using custom LabView software and visually inspected by a blinded lab member (MCB), trained in MSNA data analysis and processing.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisenone given

    The 1000 mg/day sodium diet is below the AHA recommendation of no more than 1500 mg/day for optimal cardiovascular health.

    “It is also worth noting that the 1000mg/d of sodium here is below the AHA recommendation of no more than 1500mg of sodium per day for optimal CV health.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    The RAAS may enhance sympathetically mediated vasoconstriction, so people with higher RAAS have greater vasoconstriction for a given sympathetic outflow.

    “These relations indicate that the RAAS may potentiate sympathetically-mediated vasoconstriction, such that individuals with elevated RAAS have greater vasoconstriction for a given level of sympathetic outflow.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Interpretationreasoning

    Because sodium is the main solute in extracellular fluid, sodium reduction is expected to raise RAAS to preserve extracellular fluid volume.

    “Sodium is the major solute in extracellular fluids, hence it is expected that a reduction in sodium would lead to a compensatory increase in the RAAS to maintain extracellular fluid volume.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Investigators did not know which diet each participant was assigned to.

    “Investigators were blinded to participant’s diet assignment.”
    Quote in the paperNot a substantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Study design and conductown data

    Because video recording was inadequate in three participants, leg vascular conductance results came from eight of the 11 participants with paired nerve recordings.

    “Due to an inadequate video recording in three participants, LVC is reported in eight of the 11 participants who had paired nerve recordings.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationreasoning

    Because the sodium reduction was modest and the participants were young and healthy, these findings apply more to the general population than earlier very-low-sodium studies.

    “Given the more modest sodium reduction employed in the present study, along with the fact that the population was younger and healthy, the present findings are more applicable to the general population.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim. May combine two claims.

    Study design and conductown data

    Participants ate 10-day 2300 and 1000 mg/day sodium diets in randomized order with at least a four-week washout between them.

    “The diets were 10 days each, isocaloric, matched for potassium (2500mg/d), and given in a randomized order separated by a ≥four-week washout.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing). May combine two claims.

    Study design and conductnone given

    The study protocol was approved by the University of Delaware Institutional Review Board and conformed to the Declaration of Helsinki.

    “the study protocol and procedures were approved by the Institutional Review Board of the University of Delaware and conform to the provisions of the Declaration of Helsinki.”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Interpretationown data

    In normotensive adults, lowering sodium from 2300 to 1000 mg/day stimulates the RAAS, does not raise resting sympathetic outflow, and reduces sympathetic vascular transduction.

    “These data suggest that reducing sodium from 2300 to 1000mg/day stimulates the renin- angiotensin-aldosterone system, does not increase resting basal sympathetic outflow, and reduces sympathetic vascular transduction in normotensive adults.”
    Quote in the paperSubstantial claim

  • Classified as probably not a substantial claim.

    Study design and conductown data

    The study used a randomized, crossover, controlled feeding design.

    “We performed a randomized, crossover, controlled feeding study”
    • Also stated in: § Abstract · plain
      “randomized controlled feeding study (crossover)”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Interpretationreasoning

    The modest RAAS increase from this sodium restriction may help maintain blood pressure, since the observed reduction in sympathetic transduction would otherwise be expected to lower MAP.

    “It may also be that the modest increase in RAAS observed with this level of sodium restriction act to support BP, as we observed attenuations in sympathetic transduction that would otherwise be expected to lower MAP.”
    Quote in the paperSubstantial claim
30 of 30

  • The authors state this as an assumption.

    The effect of an AHA-recommended diet on sympathetic control of the vasculature is unclear.

    “The effects of an American Heart Association-recommended diet on sympathetic regulation of the vasculature are unclear”

  • The authors state this as an assumption.

    The effect of an AHA-like low-sodium diet on MSNA and RAAS has not been established in healthy normotensive people.

    “The effects of a low sodium diet—like that recommended by the AHA—on MSNA and the RAAS have not been determined in healthy normotensive humans.”

  • The authors state this as an assumption.

    Data on how dietary sodium affects neurovascular transduction are scarce.

    “There is also a paucity of data on the effects of dietary sodium on neurovascular transduction”

  • The paper relies on this without support.

    Endothelial-derived vasodilators may reduce neurovascular transduction.

    “because endothelial-derived vasodilator compounds may blunt neurovascular transduction”

  • The authors state this as an assumption.

    This study is the first to examine or document dietary sodium-induced changes in neurovascular transduction.

    “To our knowledge, this is the first study to examine dietary sodium-induced alterations in neurovascular transduction.”
    “to our knowledge, these data are the first to document a dietary sodium-induced alteration in sympathetic transduction.”
5 of 5

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Reported sodium content conflicts with the stated low-sodium diet

    Minor

    The Results give the 1000 mg/day diet an average sodium content of 128±13 mg/day, far below the 1000 mg/day specified in Methods. This discrepancy affects the intervention underlying the paper's conclusions.

1 of 1

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Related

Authors
Babcock, M. C., Robinson, A. T., Migdal, K. U., Watso, J. C., Wenner, M. M., Stocker, S. D., & Farquhar, W. B.
Affiliations
  • University of Delaware (US)
  • University of Pittsburgh (US)
ORCID
Venue
Hypertension
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2019-03
Volume
73
Issue
3
Pages
587-593
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
DOI
10.1161/hypertensionaha.118.12074
PMC
PMC6374182
OpenAlex
W2911018560
Cited by
40
References
43
Citations by year
2025: 3 · 2024: 4 · 2023: 7 · 2022: 4 · 2021: 12 · 2020: 7 · 2019: 3
FWCI
4.94
Type
journal article
Language
en
Open access
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • American Heart Association (18POST34060020)
  • University of Delaware
  • National Institutes of Health (NIH P20 GM113125)
  • National Heart, Lung, and Blood Institute (R01HL128388)
  • National Institute of General Medical Sciences (P20GM113125)
Topics
  • Health Sciences › Nursing › Nutrition and Dietetics › Sodium Intake and Health
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
Keywords
dietary sodium reduction, muscle sympathetic nerve activity, renin-angiotensin-aldosterone system, angiotensin II, aldosterone, norepinephrine, blood pressure, cardiovascular mortality
MeSH terms
Adult, Blood Pressure, Diet, Sodium-Restricted, Dose-Response Relationship, Drug, Female, Humans, Hypertension, Male, Muscle, Smooth, Vascular, Sympathetic Nervous System, Vascular Resistance, Sodium Chloride, Dietary, Cross-Over Studies, Young Adult

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