Evidence map›Paper›PMID 25855512›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Angiotensin AT2 receptor agonist prevents salt-sensitive hypertension in obese Zucker rats.

Quaisar Ali, Sanket Patel, Tahir Hussain

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
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  5. Article
  6. Article
  7. The Angiotensin ATPharmacological reviews · 2022
    Review
  8. Bile acids and salt-sensitive hypertension: a role of the gut-liver axis.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Combining Neprilysin Inhibitor With ATFrontiers in pharmacology · 2021
    Article
  15. Article
  16. Article
  17. Article
  18. Serelaxin and the ATACS pharmacology & translational science · 2020
    Article
  19. Review
  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.

Quaisar AliDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas.
Sanket PatelDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas.ORCID http://orcid.org/0000-0003-1674-711X
Tahir HussainDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, Texas thussain@central.uh.edu.
University of Houston · 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 DK61578
6 · The paper itself

Abstract

High-sodium intake is a risk factor for the pathogenesis of hypertension, especially in obesity. The present study is designed to investigate whether angiotensin type 2 receptor (AT2R) activation with selective agonist C21 prevents high-sodium diet (HSD)-induced hypertension in obese animals. Male obese rats were treated with AT2R agonist C21 (1 mg·kg(-1)·day(-1), oral) while maintained on either normal-sodium diet (NSD; 0.4%) or HSD (4%) for 2 wk. Radiotelemetric recording showed a time-dependent increase in systolic blood pressure in HSD-fed obese rats, being maximal increase (∼27 mmHg) at day 12 of the HSD regimen. C21 treatment completely prevented the increase in blood pressure of HSD-fed rats. Compared with NSD controls, HSD-fed obese rats had greater natriuresis/diuresis and urinary levels of nitrates, and these parameters were further increased by C21 treatment. Also, C21 treatment improved glomerular filtration rate in HSD-fed rats. HSD-fed rats expressed higher level of cortical ANG II, which was reduced to 50% by C21 treatment. HSD feeding and/or C21 treatment had no effects on cortical renin activity and the expression of angiotensin-converting enzyme (ACE) and chymase, which are ANG II-producing enzymes. However, ANG(1-7) concentration and ACE2 activity in the renal cortex were reduced by HSD feeding, and C21 treatment rescued both the parameters. Also, C21 treatment reduced the cortical expression of AT1R in HSD-fed rats, but had no effect of AT2R expression. We conclude that chronic treatment with the AT2R agonist C21 prevents salt-sensitive hypertension in obese rats, and a reduction in the renal ANG II/AT1R and enhanced ACE2/ANG(1-7) levels may play a potential role in this phenomenon.

Indexed as

Angiotensin II Type 1 Receptor BlockersAnimalsBlood PressureHypertensionMaleNatriuresisObesityPeptidyl-Dipeptidase ARatsRats, ZuckerReceptor, Angiotensin, Type 2ReninSodium Chloride, DietarySodium, DietaryAngiotensin II Type 1 Receptor BlockersPeptidyl-Dipeptidase AReceptor, Angiotensin, Type 2ReninSodium Chloride, DietarySodium, Dietaryblood pressurecompound 21high-sodium dietobesity

Identifiers

PMID25855512
PMCPMC4469886
OpenAlexW1996289187

What Socratic 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 Socratic graph.