Evidence map›Paper›PMID 16390332›Full record

ArticleThe Biochemical journal2006

Involvement of the Gi/o/cGMP/PKG pathway in the AT2-mediated inhibition of outer cortex proximal tubule Na+-ATPase by Ang-(1-7).

Lucienne da Silva Lara, Fabíola Cavalcante, Flavia Axelband, Aloa Machado De Souza, Anibal Gil Lopes, Celso Caruso-Neves

Open access · bronzeAbstract read
In one paragraph

Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 72 citations in OpenAlex.

  1. Review
  2. The Angiotensin ATPharmacological reviews · 2022
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Dimerization of ATCurrent hypertension reports · 2018
    Review
  8. Review
  9. Angiotensin-(1-7) protects against the development of aneurysmal subarachnoid hemorrhage in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  10. Review
  11. Renin-angiotensin system in the kidney: What is new?World journal of nephrology · 2014
    Review
  12. Review
  13. Review
  14. Review
  15. ACE2, angiotensin-(1–7), and Mas: the other side of the coin.Pflugers Archiv : European journal of physiology · 2013
    Review
  16. The second sodium pump: from the function to the gene.Pflugers Archiv : European journal of physiology · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. Review
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

6 authors at 1 institution in 1 country.

Lucienne da Silva LaraInstituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, CCS-bloco G, 21949-900, Rio de Janeiro, RJ, Brazil.
Fabíola Cavalcante
Flavia Axelband
Aloa Machado De Souza
Anibal Gil Lopes
Celso Caruso-Neves
Universidade Federal do Rio de Janeiro · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms involved in the Ang-(1-7) [angiotensin-(1-7)] effect on sodium renal excretion remain to be determined. In a previous study, we showed that Ang-(1-7) has a biphasic effect on the proximal tubule Na+-ATPase activity, with the stimulatory effect mediated by the AT1 receptor. In the present study, we investigated the molecular mechanisms involved in the inhibition of the Na+-ATPase by Ang-(1-7). All experiments were carried out in the presence of 0.1 nM losartan to block the AT1 receptor-mediated stimulation. In this condition, Ang-(1-7) at 0.1 nM inhibited the Na+-ATPase activity of the proximal tubule by 54%. This effect was reversed by 10 nM PD123319, a specific antagonist of the AT2 receptor, and by 1 muM GDP[beta-S] (guanosine 5'-[beta-thio]diphosphate), an inhibitor of G protein. Ang-(1-7) at 0.1 M induced [35S]GTP[S] (guanosine 5'-[gamma-[35S]thio]triphosphate) binding and 1 mug/ml pertussis toxin, an inhibitor of G(i/o) protein, reversed the Ang-(1-7) effect. Furthermore, it was observed that the inhibitory effect of Ang-(1-7) on the Na+-ATPase activity was completely reversed by 0.1 microM LY83583, an inhibitor of guanylate cyclase, and by 2 muM KT5823, a PKG (protein kinase G) inhibitor, and was mimicked by 10 nM d-cGMP (dibutyryl cGMP). Ang-(1-7) increased the PKG activity by 152% and this effect was abolished by 10 nM PD123319 and 0.1 microM LY83583. Taken together, these data indicate that Ang-(1-7) inhibits the proximal tubule Na+-ATPase by interaction with the AT2 receptor that subsequently activates the G(i/o) protein/cGMP/PKG pathway.

Indexed as

Adenosine TriphosphatasesAngiotensin IAngiotensin II Type 2 Receptor BlockersAnimalsCation Transport ProteinsCyclic GMPCyclic GMP-Dependent Protein KinasesGTP-Binding Protein alpha Subunits, Gi-GoKidney CortexKidney Tubules, ProximalPeptide FragmentsReceptor, Angiotensin, Type 2Signal TransductionSwineAdenosine TriphosphatasesAngiotensin Iangiotensin I (1-7)Angiotensin II Type 2 Receptor BlockersCation Transport ProteinsCyclic GMPCyclic GMP-Dependent Protein KinasesGTP-Binding Protein alpha Subunits, Gi-GoPeptide FragmentsReceptor, Angiotensin, Type 2sodium-translocating ATPase

Identifiers

PMID16390332
PMCPMC1409686
OpenAlexW1974765210

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.