Evidence map›Paper›PMID 18095144›Full record

ArticleMolecular and cellular biochemistry2008

Oxidative stress and the genomic regulation of aldosterone-stimulated NHE1 activity in SHR renal proximal tubular cells.

Vanda Pinto, Maria João Pinho, Ulrich Hopfer, Pedro A Jose, Patrício Soares-da-Silva

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Molecular and cellular biochemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

15 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Salt-inducible kinase 1 regulates E-cadherin expression and intercellular junction stability.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2012
    Article
  11. Oxidative stress contributes to sex differences in angiotensin II-mediated hypertension in spontaneously hypertensive rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2012
    Article
  12. Genetics of salt-sensitive hypertension.Current hypertension reports · 2011
    Review
  13. Article
  14. The regulation of proximal tubular salt transport in hypertension: an update.Current opinion in nephrology and hypertension · 2009
    Review
  15. Reactive oxygen species and dopamine receptor function in essential hypertension.Clinical and experimental hypertension (New York, N.Y. : 1993) · 2009
    Review
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 3 institutions in 2 countries.

Vanda PintoFaculty of Medicine, Institute of Pharmacology and Therapeutics, Porto 4200, Portugal.
Maria João Pinho
Ulrich Hopfer
Pedro A Jose
Patrício Soares-da-Silva
Instituto Português de Oncologia Francisco Gentil · PTCase Western Reserve University · USGeorgetown University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study evaluated the effects of aldosterone upon Na+/H+ exchange (NHE) activity in immortalized proximal tubular epithelial (PTE) cells from the spontaneously hypertensive rat (SHR) and the normotensive controls (Wistar Kyoto rat; WKY). Increases in NHE activity after exposure to aldosterone occurred in time- and concentration-dependent manner in SHR PTE cells, but not in WKY PTE cells. The aldosterone-induced increases in NHE activity were prevented by spironolactone, but not by the glucocorticoid receptor antagonist Ru 38486. The presence of the mineralocorticoid receptor transcript was confirmed by PCR and NHE1, NHE2, and NHE3 proteins were detected by immunoblot analysis. Cariporide and EIPA, but not S3226, inhibited the aldosterone-induced increase in NHE activity, indicating that NHE1 is the most likely involved NHE isoform. Pretreatment of SHR PTE cells with actinomycin D attenuated the aldosterone-induced increases in NHE activity. The SHR PTE cells had an increased rate of H2O2 production when compared with WKY PTE cells. Treatment of cells with apocynin, a NADPH oxidase inhibitor, markedly reduced the rate of H2O2 production. The aldosterone-induced increase in NHE activity SHR PTE cells was completely prevented by apocynin. In conclusion, the aldosterone-induced stimulation of NHE1 activity is a genomic event unique in SHR PTE cells, which involves the activation of the mineralocorticoid receptor, but ultimately requires the availability of H2O2 in excess.

Indexed as

AldosteroneAmilorideAnimalsCell LineCytochalasin BDactinomycinGene Expression RegulationGenomeGuanidinesHydrogen-Ion ConcentrationHydrogen PeroxideImmunoblottingKidney Tubules, ProximalMethacrylatesMifepristoneOxidative Stress3-(2-(3-guanidino-2-methyl-3-oxo-propenyl)-5-methylphenyl)-N-isopropylidene-2-methyl-acrylamide dihydrochlorideAldosteroneAmiloridecariporideCytochalasin BDactinomycinethylisopropylamilorideGuanidinesHydrogen PeroxideMethacrylatesMifepristoneProtein IsoformsReceptors, MineralocorticoidRNA, MessengerSlc9a1 protein, ratSodium-Hydrogen Exchanger 1Sodium-Hydrogen ExchangersSpironolactoneSulfones

Identifiers

PMID18095144
OpenAlexW1970208355

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.