Evidence map›Paper›PMID 24760442›Full record

ReviewCurrent hypertension reports2014

New components of the renin-angiotensin system: alamandine and the MAS-related G protein-coupled receptor D.

Gisele Maia Etelvino, Antônio Augusto Bastos Peluso, Robson Augusto Souza Santos

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current hypertension reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

30 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Role of Hypertension on the Severity of COVID-19: A Review.Journal of cardiovascular pharmacology · 2021
    Review
  12. Article
  13. Recent Advances in the Endogenous Brain Renin-Angiotensin System and Drugs Acting on It.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2021
    Review
  14. Review
  15. Article
  16. Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
  17. Article
  18. Review
  19. Article
  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.

Gisele Maia EtelvinoNational Institute of Science and Technology in Nanobiopharmaceutics, Department of Physiology and Biophysics, Federal University of Minas Gerais, Av. Antonio Carlos, 6627 - ICB - UFMG, 31270-901, Belo Horizonte, MG, Brazil.
Antônio Augusto Bastos Peluso
Robson Augusto Souza Santos
Universidade Federal de Minas Gerais · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The renin-angiotensin system is an important component of the central and humoral mechanisms of blood pressure and hydro-electrolytic balance control. Angiotensin II is a key player of this system. Twenty-five years ago the first manuscripts describing the formation and actions of another peptide of the RAS, angiotensin-(1-7), were published. Since then several publications have shown that angiotensin-(1-7) is as pleiotropic as angiotensin II, influencing the functions of many organs and systems. The identification of the ACE homologue ACE2 and, a few years later, Mas, as a receptor for angiotensin-(1-7) contributed a great deal to establish this peptide as a key player of the RAS. Most of the actions of angiotensin-(1-7) are opposite to those described for angiotensin II. This has led to the concept of two arms of the RAS: one comprising ACE/AngII/AT1R and the other ACE2/Ang-(1-7)/Mas. More recently, we have described the identification of a novel component of the RAS, alamandine, which binds to the Mas-related G protein coupled receptor D. This peptide is formed by decarboxylation of the Asp residue of angiotensin-(1-7), leading to the formation of Ala as the N-terminal amino acid. Alternatively, it can be formed by hydrolysis of Ang A, by ACE2. Its effects include vasorelaxation, central effects similar to those produced by angiotensin-(1-7), blunting of isoproterenol-induced heart fibrosis, and anti-hypertensive action in SHR. The putative enzyme responsible for alamandine formation from angiotensin-(1-7) is under investigation. The identification of this novel component of the RAS opens new venues for understanding its physiological role and opens new putative therapeutic possibilities for treating cardiovascular diseases.

Indexed as

Angiotensin IAngiotensin IIAntihypertensive AgentsCardiovascular DiseasesHumansHypertensionOligopeptidesPeptide FragmentsReceptors, G-Protein-CoupledRenin-Angiotensin SystemRisk AssessmentSensitivity and SpecificityalamandineAngiotensin Iangiotensin I (1-7)Angiotensin IIAntihypertensive AgentsOligopeptidesPeptide FragmentsReceptors, G-Protein-Coupled

Identifiers

PMID24760442
OpenAlexW1970367041

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.