Evidence map›Paper›PMID 30695690›Full record

ArticleFree radical biology & medicine2019

Plasma xanthine oxidase activity is related to increased sodium and left ventricular hypertrophy in resistant hypertension.

Brittany Butts, David A Calhoun, Thomas S Denney, Steven G Lloyd, Himanshu Gupta, Krishna K Gaddam, Inmaculada Aban, Suzanne Oparil, Paul W Sanders, Rakesh Patel and 2 more

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
2.1field-weighted citation impact, top 13% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 19 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Brittany ButtsDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA; Nell Hodgson Woodruff School of Nursing, Emory University, USA.
David A CalhounDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA.
Thomas S DenneyDepartment of Electrical and Computer Engineering, Auburn University, USA.
Steven G LloydDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA.
Himanshu GuptaDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA; Birmingham Department of Veterans Affairs Medical Center, USA.
Krishna K GaddamDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA.
Inmaculada AbanDepartment of Biostatistics, University of Alabama at Birmingham, USA.
Suzanne OparilDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA.
Paul W SandersDivision of Nephrology, University of Alabama at Birmingham School of Medicine, USA.
Rakesh PatelCenter for Free Radical Biology and Department of Pathology, University of Alabama at Birmingham, USA.
James F CollawnDepartment of Cell, Developmental, and Integrative Biology, University of Alabama at Birmingham, USA.
Louis J Dell'ItaliaDivision of Cardiovascular Disease, University of Alabama at Birmingham School of Medicine, USA; Birmingham Department of Veterans Affairs Medical Center, USA. Electronic address: louis.dellitalia@va.gov.
University of Alabama at Birmingham · USAuburn University · USBirmingham VA Medical Center · USEmory University · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MEHTA, RAVINDRA L. · 2008 to 2022
$18.3M
The Impact on Diabetes on Left Ventricular RemodelingP50HL077100 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI DELL'LTALIA, LOUIS · 2005 to 2009
$16.5M
Interdisciplinary Training in Pathobiology and Rehabilitation Medicine.T32HD071866 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI JAMES RIMMER, Anna E. Thalacker-Mercer · 2012 to 2026
$4.8M
The essentiality of serine and glycine for skeletal muscle regeneration in agingR01AG075059 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI THALACKER-MERCER, ANNA E. · 2022 to 2025
$1.5M
Symptoms and Skeletal Muscle in Persons with Heart Failure with Preserved Ejection FractionF32NR017322 · NINR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BUTTS, BRITTANY · 2017 to 2018
$68k
Novel Regulators of Vascular DiseaseIP1BX001595 · VA · BIRMINGHAM VA MEDICAL CENTER · PI AGARWAL, ANUPAM, CHEN, YABING · 2013 to 2016
–
BLRD VA I01 BX004426NHLBI NIH HHS P50 HL077100NIA NIH HHS R01 AG075059NICHD NIH HHS T32 HD071866NIDDK NIH HHS P30 DK079626NINR NIH HHS F32 NR017322
6 · The paper itself

Abstract

backgroundThe extra-renal effects of aldosterone on left ventricular (LV) structure and function are exacerbated by increased dietary sodium in persons with hypertension. Previous studies demonstrated endothelial dysfunction and increased oxidative stress with high salt diet in normotensive salt-resistant subjects. We hypothesized that increased xanthine oxidase (XO), a product of endothelial cells, is related to 24-h urinary sodium and to LV hypertrophy and function in patients with resistant hypertension (RHTN).

methodsThe study group included persons with RHTN (n = 91), defined as a blood pressure > 140/90 mmHg on ≥ 3 medications at pharmacologically effective doses. Plasma XO activity and 24-h urine were collected, and cardiac magnetic resonance imaging (MRI) was performed to assess LV function and morphology. Sixty-seven normotensive persons on no cardiovascular medications served as controls. A subset of RHTN (n = 19) received spironolactone without salt restriction for six months with follow-up XO activity measurements and MRI analyses.

resultsXO activity was increased two-fold in RHTN vs. normal and was positively correlated with LV mass, LV diastolic function, and 24-h urinary sodium. In RHTN patients receiving spironolactone without salt restriction, LV mass decreased, but LV diastolic function and XO activity did not improve. Baseline urinary sodium was positively associated with rate of change of LV mass to volume ratio and the LV E/A ratio.

conclusionsThese results demonstrate a potential role of endothelium-derived oxidative stress and excess dietary salt in the pathophysiology of LV hypertrophy and diastolic dysfunction in persons with RHTN unaffected by the addition of spironolactone.

Indexed as

AdultCase-Control StudiesFemaleHumansHypernatremiaHypertensionHypertrophy, Left VentricularMaleMiddle AgedPrognosisRetrospective StudiesSodiumXanthine OxidaseSodiumXanthine OxidaseDietary sodiumLeft ventricular hypertrophyOxidative stressXanthine oxidase

Identifiers

PMID30695690
PMCPMC6588431
OpenAlexW2912089560

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.