Evidence map›Paper›PMID 23529167›Full record

ArticleHypertension (Dallas, Tex. : 1979)2013

Enhanced angiotensin receptor-associated protein in renal tubule suppresses angiotensin-dependent hypertension.

Hiromichi Wakui, Kouichi Tamura, Shin-Ichiro Masuda, Yuko Tsurumi-Ikeya, Megumi Fujita, Akinobu Maeda, Masato Ohsawa, Kengo Azushima, Kazushi Uneda, Miyuki Matsuda and 7 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.2field-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

35 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  3. Article
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  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. ATRAP, a receptor-interacting modulator of kidney physiology, as a novel player in blood pressure and beyond.Hypertension research : official journal of the Japanese Society of Hypertension · 2022
    Review
  12. Article
  13. Aristolochic Acid Induces Renal Fibrosis and Senescence in Mice.International journal of molecular sciences · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 4 institutions in 2 countries.

Hiromichi WakuiDepartment of Medical Science and Cardiorenal Medicine, Yokohama City University Graduate School of Medicine, 3-9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan.
Kouichi Tamura
Shin-Ichiro Masuda
Yuko Tsurumi-Ikeya
Megumi Fujita
Akinobu Maeda
Masato Ohsawa
Kengo Azushima
Kazushi Uneda
Miyuki Matsuda
Kenichiro Kitamura
Shinichi Uchida
Yoshiyuki Toya
Hiroyuki Kobori
Kiyotaka Nagahama
Akio Yamashita
Satoshi Umemura
Yokohama City University · JPKumamoto University · JPTokyo Medical and Dental University · JPTulane University · US

Funding

Intrarenal Augmentation of Angiotensinogen by Ang IIR01DK072408 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2006 to 2010
$1.2M
NIDDK NIH HHS R01 DK072408
6 · The paper itself

Abstract

We have previously shown that angiotensin II type 1 receptor-associated protein (ATRAP/Agtrap) interacts with the angiotensin II type 1 receptor and promotes constitutive internalization of the receptor so as to inhibit the pathological activation of its downstream signaling but preserve baseline physiological signaling activity. The present study was designed to investigate the role of renal ATRAP in angiotensin II-dependent hypertension. We generated transgenic mice dominantly expressing ATRAP in the renal tubules, including renal distal tubules. The renal ATRAP transgenic mice exhibited no significant change in blood pressure at baseline on normal salt diet. However, in the renal ATRAP transgenic mice compared with wild-type mice, the following took place: (1) the development of high blood pressure in response to angiotensin II infusion was significantly suppressed based on radiotelemetry, (2) the extent of daily positive sodium balance was significantly reduced during angiotensin II infusion in metabolic cage analysis, and (3) the renal Na+ -Cl- cotransporter activation and α-subunit of the epithelial sodium channel induction by angiotensin II infusion were inhibited. Furthermore, adenoviral overexpression of ATRAP suppressed the angiotensin II-mediated increase in the expression of α-subunit of the epithelial sodium channel in mouse distal convoluted tubule cells. These results indicate that renal tubule-dominant ATRAP activation provokes no evident effects on blood pressure at baseline but exerts an inhibitory effect on the pathological elevation of blood pressure in response to angiotensin II stimulation, thereby suggesting that ATRAP is a potential target of interest in blood pressure modulation under pathological conditions.

Indexed as

Gene Expression RegulationAdaptor Proteins, Signal TransducingAngiotensin IIAnimalsBlood PressureBlotting, WesternDisease Models, AnimalDNAHypertensionKidney Tubules, DistalMaleMiceMice, TransgenicPolymerase Chain ReactionRenin-Angiotensin SystemAdaptor Proteins, Signal TransducingAgtrap protein, mouseAngiotensin IIDNAangiotensin IIangiotensin receptorsbasic sciencegene expression/regulationhypertension (kidney)membrane transport/ion channelsreceptors

Identifiers

PMID23529167
PMCPMC3657390
OpenAlexW2165843485

What Socratic 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 Socratic graph.