Evidence map›Paper›PMID 32327962›Full record

ArticleSignal transduction2006

Hypothesized and found mechanisms for potentiation of bradykinin actions.

Sylvia Mueller, Inge Paegelow, Siegmund Reissmann

Open access · bronzeAbstract read
In one paragraph

Article in Signal transduction, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 31% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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 2 institutions in 1 country.

Sylvia MuellerInstitute of Biochemistry and Biophysics, Biological and Pharmaceutical Faculty, Friedrich-Schiller-University Jena, Jena, Germany.
Inge PaegelowDepartment of Experimental and Clinical Pharmacology and Toxicology, University of Rostock, Rostock, Germany.
Siegmund ReissmannInstitute of Biochemistry and Biophysics, Biological and Pharmaceutical Faculty, Friedrich-Schiller-University Jena, Jena, Germany.
Friedrich Schiller University Jena · DEUniversity of Rostock · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Potentiation of hormone actions can occur by different mechanisms, including inhibition of degrading enzymes, interaction with the hormone receptor leading to stabilization of bioactive conformation or leading to receptor homo- and hetero-oligomerization, receptor phosphorylation and dephosphorylation or can occur by directly influencing the signal transduction and ion channels. In this review the potentiation of bradykinin actions in different systems by certain compounds will be reviewed. Despite many long years of experimental research and investigation the mechanisms of potentiating action remain not fully understood. One of the most contradictory findings are the distinct differences between the inhibition of the angiotensin I-converting enzyme and the potentiation of the bradykinin induced smooth muscle reaction. Contradictory findings and hypothesized mechanisms in the literature are discussed in this review and in some cases compared to own results. Investigation of potentiating actions was extended from hypotension, smooth muscle reaction and cellular actions to activation of immunocompetent cells. In our opinion the potentiation of bradykinin action can occur by different mechanisms, depending on the system and the applied potentiating factor used.

Indexed as

Angiotensin I‐converting enzymeBradykinin B1 and B2 receptorsCrosstalkPolymorphonuclear leukocytesPotentiation

Identifiers

PMID32327962
PMCPMC7169587
OpenAlexW2151828499

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.