Evidence map›Paper›PMID 23336117›Full record

ReviewClinical and experimental pharmacology & physiology2013

Role of angiotensin AT(2) receptors in natriuresis: Intrarenal mechanisms and therapeutic potential.

Robert M Carey, Shetal H Padia

Abstract readReview
In one paragraph

Review in Clinical and experimental pharmacology & physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.2field-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

22 citing papers in PubMed, 45 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. The Dopamine DHypertension (Dallas, Tex. : 1979) · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Interaction of the renin angiotensin and cox systems in the kidney.Frontiers in bioscience (Scholar edition) · 2016
    Review
  16. Article
  17. Review
  18. Article
  19. Angiotensin II and vascular injury.Current hypertension reports · 2014
    Review
  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

2 authors at 1 institution in 1 country.

Robert M CareyDivision of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville, VA 22908, USA. rmc4c@virginia.edu
Shetal H Padia
University of Virginia Health System · US

Funding

Renal AT2 Receptors in HypertensionR01HL095796 · NHLBI · UNIVERSITY OF VIRGINIA · PI CAREY, ROBERT MUNSON · 2010 to 2013
$1.7M
NHLBI NIH HHS R01 HL095796
6 · The paper itself

Abstract

The renin-angiotensin system is a coordinated hormonal cascade critical for the regulation of blood pressure (BP) and kidney function. Angiotensin (Ang) II, the major angiotensin effector peptide, binds to two major receptors, namely AT1 and AT2 receptors. The AT1 receptors engender antinatriuresis and raise BP, whereas AT2 receptors oppose these effects, inducing natriuresis and reducing BP. There is high AT2 receptor expression in the adult kidney, especially in the proximal tubule. In AT2 receptor-null mice, long-term AngII infusion results in pressor and antinatriuretic hypersensivivity compared with responses in wild-type mice. The major endogenous receptor ligand for AT2 receptor-mediated natriuretic responses appears to be des-aspartyl(1) -AngII (AngIII) instead of AngII. Recent studies have demonstrated that AngII requires metabolism to AngIII by aminopeptidase A to induce natriuresis and that inhibition of aminopeptidase N increases intrarenal AngIII and augments AngIII-induced natriuresis. The renal dopaminergic system is another important natriuretic pathway. Renal proximal tubule the D1 and D5 receptor subtypes (D1 -like receptors (D1LIKE R)) control approximately 50% of basal sodium excretion. Recently, we have found that natriuresis induced by proximal tubule D1LIKE R requires AT2 receptor activation and that D1LIKE R stimulation induces recruitment of AT2 receptors to the apical plasma membrane via a cAMP-dependent mechanism. Initial studies using the potent AT2 receptor non-peptide agonist Compound 21 demonstrate natriuresis in both the presence and absence of AT1 receptor blockade, indicating the therapeutic potential of this compound in fluid-retaining states and hypertension.

Indexed as

AnimalsKidneyNatriuresisReceptor, Angiotensin, Type 2Renin-Angiotensin SystemSodiumReceptor, Angiotensin, Type 2Sodiumangiotensindopaminedopamine receptorshypertensionnatriuresisreceptorsrenin-angiotensin system

Identifiers

PMID23336117
PMCPMC4011555
OpenAlexW2133550871

What OpenQuestion holds

Textmetadata
LicenceTDM
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.