Evidence map›Paper›PMID 22592638›Full record

ArticleAmerican journal of physiology. Renal physiology2012

High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT(2)R-MasR axis in obese Zucker rats.

Preethi Samuel, Quaisar Ali, Rifat Sabuhi, Yonnie Wu, Tahir Hussain

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing 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

23 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Article
  10. Relationships between urinary electrolytes excretion and central hemodynamics, and arterial stiffness in hypertensive patients.Hypertension research : official journal of the Japanese Society of Hypertension · 2017
    Article
  11. Article
  12. Article
  13. Plasma Vitamin D Level and Change in Albuminuria and eGFR According to Sodium Intake.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Observational
  14. Article
  15. Review
  16. Article
  17. Article
  18. ACE and ACE2 in kidney disease.World journal of nephrology · 2015
    Review
  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

5 authors at 2 institutions in 1 country.

Preethi SamuelDepartment of Pharmacal Sciences, Harrison School of Pharmacy, Auburn University, Auburn, AL 36849, USA.
Quaisar Ali
Rifat Sabuhi
Yonnie Wu
Tahir Hussain
University of Houston · USAuburn University · US

Funding

Renal Angiotensin ll Receptor Function in ObesityR01DK061578 · NIDDK · UNIVERSITY OF HOUSTON · PI HUSSAIN, TAHIR · 2003 to 2020
$4.3M
NIDDK NIH HHS R01 DK061578NIDDK NIH HHS R01 DK-61578
6 · The paper itself

Abstract

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT(1)R) vs. AT(2)-ACE2-angiotensinogen (Ang) (1-7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT(1A/B)R, ACE, AT(2)R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT(1B)R increased, renin decreased, and ACE2, AT(2)R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT(2)R, and MasR, and no changes in renin and AT(1)R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT(2)R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT(1)R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

Indexed as

ActinsAngiotensin-Converting Enzyme 2Angiotensin IAngiotensin IIAngiotensinogenAnimalsBlood PressureChromatography, High Pressure LiquidHypertension, RenalKidneyKidney CortexMaleMass SpectrometryObesityPeptide FragmentsPeptidyl-Dipeptidase AAce2 protein, ratActinsAngiotensin-Converting Enzyme 2Angiotensin Iangiotensin I (1-7)Angiotensin IIAngiotensinogenPeptide FragmentsPeptidyl-Dipeptidase AProto-Oncogene MasProto-Oncogene ProteinsReceptor, Angiotensin, Type 2Receptors, G-Protein-CoupledReninSodium, Dietary

Identifiers

PMID22592638
PMCPMC3433866
OpenAlexW2120897878

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.