Cited by 211Blood Pressure and Hypertension StudiesDiabetes, Cardiovascular Risks, and LipoproteinsCardiovascular and exercise physiology

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index; 4 of the 56 sources its claims cite were checked for support.

Sympathetic Neural Activation in Nondiabetic Metabolic Syndrome and Its Further Augmentation by Hypertension

Huggett, Robert J., Burns, Joanna, Mackintosh, Alan F., Mary, David A.S.G.·2004·Hypertension

Abstract

Hypertension is a major cardiovascular risk factor in the metabolic syndrome (MS) in which the presence of insulin resistance, glucose intolerance, abnormal lipoprotein metabolism, and central obesity all confer an increased risk. Because essential hypertension (EHT), insulinemia, and visceral fat are associated with sympathetic hyperactivity, which is itself known to increase cardiovascular risk, the aim of this study was to see if MS is a state of sympathetic nerve hyperactivity and if the additional presence of EHT intensifies this hyperactivity. In 69 closely matched subjects, comprising hypertensive MS (MS+EHT, 18), normotensive MS (MS-EHT, 17), hypertensives without MS (EHT, 16), and normotensive controls without MS (NC, 18), we measured resting muscle sympathetic nerve activity (MSNA) as assessed from multiunit discharges and from single units with defined vasoconstrictor properties (s-MSNA). The s-MSNA in MS+EHT (76±3.1 impulses/100 beats) was greater (at least P <0.01) than in MS-EHT (62±3.2 impulses/100 beats) and in EHT (60±2.3 impulses/100 beats), and all these were significantly greater (at least P <0.01) than in NC (46±2.7 impulse/100 beats). The multi-unit MSNA followed a similar trend. These findings suggest that MS is a state of sympathetic nerve hyperactivity and that the additional presence of hypertension further intensifies this hyperactivity. The degree of sympathetic hyperactivity seen in this study could be argued at least partly to contribute to the higher cardiovascular risk and metabolic abnormalities seen in MS+EHT patients.

Overview

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TL;DR

In nondiabetic metabolic syndrome, resting sympathetic nerve activity is increased, and the additional presence of hypertension further augments it. The authors conclude this sympathetic hyperactivity may contribute to higher cardiovascular risk and metabolic abnormalities in MS+EHT.

Key findings

  • Resting single-unit muscle sympathetic nerve activity (s-MSNA) was 76±3.1 impulses/100 beats in MS+EHT, greater than 62±3.2 in MS-EHT and 60±2.3 in EHT (at least P<0.01), and all three groups exceeded NC at 46±2.7 impulses/100 beats (at least P<0.01); multiunit MSNA followed a similar trend.
  • MS+EHT had the highest sympathetic activity, significantly greater than MS-EHT, which was similar to EHT; s-MSNA hyperactivity was increased by ≈65% in MS+EHT and ≈35% in MS-EHT versus NC.
  • MS groups had greater fasting glucose, insulin, HOMA-IR, triglycerides, and lower HDL cholesterol than EHT and NC; the only difference between MS+EHT and MS-EHT was slightly greater triglycerides in MS+EHT.
  • Plasma insulin and HOMA-IR positively correlated with s-MSNA and MSNA in MS+EHT (r 0.41–0.45; at least P<0.04) and MS-EHT (r 0.49–0.53; at least P<0.02); no significant correlations were found with waist circumference, waist/hip ratio, fasting glucose, triglycerides, or HDL (r −0.34 to 0.42; at least P>0.05).

Methods

  • Cross-sectional comparison of 69 white subjects with complete data (from 72 examined; 3 excluded because stable single-unit microneurographic data could not be obtained): MS+EHT n=18, MS-EHT n=17, EHT n=16, NC n=18. MS was defined by NCEP ATP III criteria; diabetes was excluded.
  • Resting postganglionic muscle sympathetic nerve activity was recorded from the right peroneal nerve by microneurography, quantified as multiunit MSNA and single-unit s-MSNA with vasoconstrictor properties; simultaneous ECG, Finometer arterial pressure, strain-gauge calf blood flow, and calf vascular resistance were measured, and baroreceptor reflex sensitivity was obtained from Valsalva.
  • One-way ANOVA with Newman-Keuls post-tests compared groups; least-square technique assessed linear relationships; P<0.05 was significant; data are mean±SEM.

Limitations

  • Stated: antihypertensive therapy differed between groups and was not withdrawn; the authors state they cannot entirely exclude an influence of ACE inhibitors, ARBs, thiazide diuretics, or beta-blockers, although they argue these agents could not entirely cause the excessive sympathetic hyperactivity.
  • Stated: findings may not extrapolate beyond white subjects because insulinemia and sympathetic nerve activity can differ by ethnicity; the authors also state there may be differences in sympathetic output to regions other than the leg.
  • Stated/evident: the study is cross-sectional and the authors state their findings do not establish a causal relationship between MS and sympathetic activity; no longitudinal or interventional causal test was performed.

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Integrity signals

Registry

Crossref · 10.1161/01.hyp.0000147893.08533.d8

Cites

44 of 44 references verified0 citation errors · 0 not checkable

Statistics

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Verification

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29 Not checked yet · 16 Own result · 9 Own method · 7 Own interpretation · 2 Partly supported · accuracy not yet measured

Verify all 52 references — free account
  • It may state two separate claims as one. 18
  • The quote only partly states this claim. 1
  • Probably not a substantial claim. 15
28 of 28
  • The paper relies on this without support.

    s-MSNA reflects the mean resting sympathetic nerve frequency supplying the peripheral vessels.

    “We measured both s-MSNA and MSNA frequencies because s-MSNA reflects the mean resting sympathetic nerve frequency supplying the peripheral vessels.”
1 of 1

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Citations

Cites

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Research works printed but not linked: 5

  1. 10.1161/circ.100.12.1305 · DOI
  2. 10.1161/hyp.34.4.724 · DOI
  3. 10.1161/hyp.36.4.538 · DOI
  4. 10.1161/hyp.27.2.276 · DOI
  5. 10.1161/hyp.36.4.531 · DOI

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Metadata

Authors
Huggett, R. J., Burns, J., Mackintosh, A. F., & Mary, D. A. S. G.
Affiliations
St James's University Hospital (GB)
Venue
Hypertension
Published
2004-12
Volume
44
Issue
6
Pages
847-852
ISSN
  • 0194-911X (ISSN-L)
  • 1524-4563
OpenAlex
W2166344703
Cited by
211
References
44
Citations by year
2026: 2 · 2025: 2 · 2024: 2 · 2023: 7 · 2022: 5 · 2021: 8 · 2020: 3 · 2019: 5 · 2018: 5 · 2017: 10 · 2016: 15 · 2015: 15 · 2014: 15 · 2013: 10 · 2012: 17
FWCI
8.92
Type
journal article
Language
en
Open access
closed
Locations
  • Hypertension (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
  • Health Sciences › Medicine › Physiology (medical) › Cardiovascular and exercise physiology
Keywords
metabolic syndrome, essential hypertension, muscle sympathetic nerve activity, cardiovascular risk, visceral fat, insulin resistance, non-diabetic patients
MeSH terms
Anthropometry, Blood Pressure, Electrodiagnosis, Female, Humans, Hypertension, Male, Middle Aged, Sympathetic Nervous System, Metabolic Syndrome

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