Evidence map›Paper›PMID 25740064›Full record

ReviewJournal of endocrinological investigation2015

Mechanistic approach to the pathophysiology of target organ damage in hypertension from studies in a human model with characteristics opposite to hypertension: Bartter's and Gitelman's syndromes.

L A Calò, G Maiolino

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of endocrinological investigation, 2015. 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
–field-weighted citation impact
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.

  1. Review
  2. Article
  3. Article
  4. Characteristics and Follow-Up of 13 pedigrees with Gitelman syndrome.Journal of endocrinological investigation · 2019
    Article
  5. Article
  6. Article
  7. Review
  8. 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

2 authors.

L A CalòDepartment of Medicine, Nephrology and Hypertension, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy. renzcalo@unipd.it.
G MaiolinoDepartment of Medicine, Nephrology and Hypertension, University of Padova, Via Giustiniani, 2, 35128, Padua, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionExtensive studies using Bartter's/Gitelman's syndrome patients have provided insights into the angiotensin II (Ang II) signaling pathways involved in the regulation of vascular tone and cardiovascular-renal remodeling. The renin-angiotensin-aldosterone system is activated in these syndromes, however, patients do not develop hypertension and cardiovascular remodeling and clinically manifest conditions opposite to hypertension. The short- and the long-term signaling of Ang II remains an important matter of investigation to shed light on mechanisms responsible for the pathophysiology of hypertension and its long-term complications. The long-term signaling of Ang II is involved in the pathophysiology of cardiovascular-renal remodeling and inflammatory responses in which the balance between RhoA/Rho kinase pathway and NO system plays a crucial role. METHODS AND

resultsIn this brief review, the results of our studies in Bartter's and Gitelman's syndromes are reported on these processes.

conclusionsThe information obtained from these studies can clarify, confirm or be used to extend the biochemical mechanisms responsible for the pathophysiology of hypertension and its long-term complications and could offer further chances to identify additional potential significant targets of therapy.

Indexed as

Bartter SyndromeGitelman SyndromeHumansHypertensionAngiotensin II signalingBartter’s syndromeCardiovascular–renal remodelingGitelman’s syndromeHypertensionNitric oxideRho kinase

Identifiers

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.