Evidence map›Paper›PMID 20226958›Full record

ReviewProgress in cardiovascular diseases

Aldosterone: role in the cardiometabolic syndrome and resistant hypertension.

Adam Whaley-Connell, Megan S Johnson, James R Sowers

Registry-linked trialOpen access · greenAbstract readReview
In one paragraph

Review in Progress in cardiovascular diseases. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04213963 (Prospective Cross-sectional Study on Prevalence of Primary Aldosteronism in Resistant Hypertension and Association With Cardiometabolic Complications), which is not on this map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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.

NCT04213963 unknown statusnot on this map

Prospective Cross-sectional Study on Prevalence of Primary Aldosteronism in Resistant Hypertension and Association With Cardiometabolic Complications

TypeobservationalSponsorUniversity of Turin, ItalyRan2011 to 2025Enrolled100ConditionsResistant Hypertension, Primary Aldosteronism, Refractory Hypertension, Hypertensive End-Organ Damage
3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 150 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Study of aldosterone synthase inhibition as an add-on therapy in resistant hypertension.Journal of clinical hypertension (Greenwich, Conn.) · 2013
    Trial
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Antidiabetic effect of an engineered bacteriumSynthetic and systems biotechnology · 2021
    Article
  12. Article
  13. Mineralocorticoid receptors in the pathogenesis of insulin resistance and related disorders: from basic studies to clinical disease.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

3 authors at 1 institution in 1 country.

Adam Whaley-ConnellDepartment of Internal Medicine, University of Missouri-Columbia School of Medicine, Columbia, MO 65212, USA.
Megan S Johnson
James R Sowers
University of Missouri · US

Funding

ANG II OPPOSES INS MEDIATED VASORELAXATION &GLU UTILZAR01HL073101 · NHLBI · UNIVERSITY OF MISSOURI-COLUMBIA · PI SOWERS, JAMES RUSSELL · 2004 to 2013
$2.7M
NHLBI NIH HHS R01 HL073101NHLBI NIH HHS R01 HL73101-01A1
6 · The paper itself

Abstract

The prevalence of diabetes, hypertension, and cardiovascular disease (CVD) and chronic kidney disease (CKD) is increasing in concert with obesity. Insulin resistance, metabolic dyslipidemia, central obesity, albuminuria. and hypertension commonly cluster to comprise the cardiometabolic syndrome (CMS). Emerging evidence supports a shift in our understanding of the crucial role of elevated serum aldosterone in promoting insulin resistance and resistant hypertension. Aldosterone enhances tissue generation of oxygen free radicals and systemic inflammation. This increase in oxidative stress and inflammation, in turn, contributes to impaired insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. In this context, recent investigation indicates that hyperaldosteronism, which is often associated with obesity, contributes to impaired pancreatic beta-cell function as well as diminished skeletal muscle insulin metabolic signaling. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated, in part, by aldosterone's nongenomic as well as genomic signaling through the mineralocorticoid receptor (MR). In the CMS, there are increased circulating levels of glucocorticoids, which can also activate MR signaling in cardiovascular, adipose, skeletal muscle, neuronal, and liver tissue. Furthermore, there is increasing evidence that fat tissue produces a lipid soluble factor that stimulates aldosterone production from the adrenal zona glomerulosa. Recently, we have learned that MR blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation as well as reduces the progression of CVD and CKD. In summary, aldosterone excess exerts detrimental metabolic effects that contribute to the development of the CMS and resistant hypertension as well as CVD and CKD.

Indexed as

AldosteroneAnimalsAntihypertensive AgentsBlood PressureDrug ResistanceEndothelium, VascularHeartHumansHyperaldosteronismHypertensionInsulin ResistanceKidneyMetabolic SyndromeMineralocorticoid Receptor AntagonistsReceptors, MineralocorticoidRisk FactorsAldosteroneAntihypertensive AgentsMineralocorticoid Receptor AntagonistsReceptors, Mineralocorticoid

Identifiers

PMID20226958
PMCPMC2841057
OpenAlexW2056310243

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.