Evidence map›Paper›PMID 29212952›Full record

ArticleJCI insight2017

Dysregulated aldosterone secretion in persons of African descent with endothelin-1 gene variants.

Jia W Tan, Tina Gupta, Worapaka Manosroi, Tham M Yao, Paul N Hopkins, Jonathan S Williams, Gail K Adler, Jose R Romero, Gordon H Williams

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

7 citing papers in PubMed, 11 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Kidney-specific KO of the circadian clock protein PER1 alters renal NaAmerican journal of physiology. Renal physiology · 2022
    Article
  5. Article
  6. Review
  7. Article
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

9 authors at 2 institutions in 1 country.

Jia W TanDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Tina GuptaDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Worapaka ManosroiDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Tham M YaoDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Paul N HopkinsCardiovascular Genetics Unit, Cardiology Division, Department of Medicine, University of Utah School of Medicine, Salt Lake City, Utah, USA.
Jonathan S WilliamsDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Gail K AdlerDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Jose R RomeroDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Gordon H WilliamsDivision of Endocrinology, Diabetes and Hypertension, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Brigham and Women's Hospital · USHarvard University · US

Funding

HARVARD CLINICAL AND TRANSLATIONAL SCIENCE CENTER (UL1)UL1RR025758 · NCRR · HARVARD MEDICAL SCHOOL · PI NADLER, LEE MARSHALL · 2008 to 2011
$91.4M
Zoledronic Acid in Treatment of Osteoporosis in PostmenoM01RR002635 · NCRR · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 1985 to 2008
$48.4M
SCOR MOLECULAR GENETICS OF HYPERTENSIONP50HL055000 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI SEELY, ELLEN W · 1996 to 2005
$13.5M
TRAINING PROGRAM IN HYPERTENSIONT32HL007609 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 1985 to 2022
$10.2M
Genetics of Human HypertensionR01HL086907 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 2007 to 2011
$3.5M
Caveolin-1 and vascular dysfunctionR01HL104032 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI POJOGA, LUMINITA · 2010 to 2014
$2.1M
Aldosteron, Intracellular Leukocyte Magnesium and Inflammation in DiabetesR01HL096518 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ROMERO, JOSE R · 2009 to 2012
$1.9M
Mechanisms of Aldosterone Induced Cardiovascular DamageR01HL069208 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI WILLIAMS, GORDON H · 2003 to 2006
$1.8M
Aldosterone and Diabetic Cardiovascular Disease: Research and Mentoring ProgamK24HL103845 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI ADLER, GAIL KURR · 2011 to 2021
$1.6M
NCRR NIH HHS M01 RR002635NCRR NIH HHS UL1 RR025758NHLBI NIH HHS K24 HL103845NHLBI NIH HHS P50 HL055000NHLBI NIH HHS R01 HL069208NHLBI NIH HHS R01 HL086907NHLBI NIH HHS R01 HL096518NHLBI NIH HHS R01 HL104032NHLBI NIH HHS T32 HL007609
6 · The paper itself

Abstract

Compared with persons of European descent (ED), persons of African descent (AD) have lower aldosterone (ALDO) levels, with the assumption being that the increased cardiovascular disease (CVD) risk associated with AD is not related to ALDO. However, the appropriateness of the ALDO levels for the volume status in AD is unclear. We hypothesized that, even though ALDO levels are lower in AD, they are inappropriately increased, and therefore, ALDO could mediate the increased CVD in AD. To test this hypothesis, we analyzed data from HyperPATH - 1,788 individuals from the total cohort and 765 restricted to ED-to-AD in a 2:1 match and genotyped for the endothelin-1 gene (EDN1). Linear regression analyses with adjustments were performed. In the total and restricted cohorts, PRA, ALDO, and urinary potassium levels were significantly lower in AD. However, in the AD group, greater ALDO dysregulation was present as evidenced by higher ALDO/plasma renin activity (PRA) ratios (ARR) and sodium-modulated ALDO suppression-to-stimulation indices. Furthermore, EDN1 minor allele carriers had significantly greater ARRs than noncarriers but only in the AD group. ARR levels were modulated by a significant interaction between EDN1 and AD. Thus, EDN1 variants may identify particularly susceptible ADs who will be responsive to treatment targeting ALDO-dependent pathways (e.g., mineralocorticoid-receptor antagonists).

Indexed as

AdultAldosteroneAnimalsBlack PeopleCells, CulturedCohort StudiesEndothelin-1FemaleGenotypeHumansMaleMiddle AgedPotassiumRats, WistarReninSodium Chloride, DietaryAldosteroneEndothelin-1PotassiumReninSodium Chloride, DietaryCardiovascular diseaseEndocrinologyEpigeneticsGeneticsHypertension

Identifiers

PMID29212952
PMCPMC5752283
OpenAlexW2775201311

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.