Evidence map›Paper›PMID 33280408›Full record

ArticleHypertension (Dallas, Tex. : 1979)2021

Site-1 Protease-Derived Soluble (Pro)Renin Receptor Contributes to Angiotensin II-Induced Hypertension in Mice.

Ye Feng, Kexin Peng, Renfei Luo, Fei Wang, Tianxin Yang

Open access · hybridAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

20 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Kidney Renin-Angiotensin System: Lost in a RAS Cascade.Hypertension (Dallas, Tex. : 1979) · 2024
    Article
  5. Functional Roles of Furin in Cardio-Cerebrovascular Diseases.ACS pharmacology & translational science · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021
    Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Ye FengFrom the Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City.
Kexin PengFrom the Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City.
Renfei LuoFrom the Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City.
Fei WangFrom the Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City.
Tianxin YangFrom the Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City.
University of Utah · US

Funding

Role of (pro)renin receptor in aldosterone signaling in the kidneyR01HL139689 · NHLBI · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2018 to 2021
$2.3M
Interaction of (pro)renin receptor and PPARy in regulation of plasma volumeR01HL135851 · NHLBI · UNIVERSITY OF UTAH · PI YANG, TIANXIN · 2017 to 2021
$2.3M
BLRD VA I01 BX002817BLRD VA I01 BX004871BLRD VA IK6 BX005223NHLBI NIH HHS R01 HL135851NHLBI NIH HHS R01 HL139689
6 · The paper itself

Abstract

Activation of PRR ([pro]renin receptor) contributes to enhancement of intrarenal RAS and renal medullary α-ENaC and thus elevated blood pressure during Ang II (angiotensin II) infusion. The goal of the present study was to test whether such action of PRR was mediated by sPRR (soluble PRR), generated by S1P (site-1 protease), a newly identified PRR cleavage protease. F1 B6129SF1/J mice were infused for 6 days with control or Ang II at 300 ng/kg per day alone or in combination with S1P inhibitor PF-429242 (PF), and blood pressure was monitored by radiotelemetry. S1P inhibition significantly attenuated Ang II-induced hypertension accompanied with suppressed urinary and renal medullary renin levels and expression of renal medullary but not renal cortical α-ENaC expression. The effects of S1P inhibition were all reversed by supplement with histidine-tagged sPRR termed as sPRR-His. Ussing chamber technique was performed to determine amiloride-sensitive short-circuit current, an index of ENaC activity in confluent mouse cortical collecting duct cell line cells exposed for 24 hours to Ang II, Ang II + PF, or Ang II + PF + sPRR-His. Ang II-induced ENaC activity was blocked by PF, which was reversed by sPRR-His. Together, these results support that S1P-derived sPRR mediates Ang II-induced hypertension through enhancement of intrarenal renin level and activation of ENaC.

Indexed as

Angiotensin IIAnimalsBlood PressureHypertensionMiceProprotein ConvertasesProrenin ReceptorPyrrolidinesReceptors, Cell SurfaceReninRenin-Angiotensin SystemSerine EndopeptidasesAngiotensin IImembrane-bound transcription factor peptidase, site 1PF-429242Proprotein ConvertasesProrenin ReceptorPyrrolidinesReceptors, Cell SurfaceReninSerine Endopeptidasesamilorideangiotensin IIblood pressureepithelial sodium channelsrenin

Identifiers

PMID33280408
PMCPMC7803453
OpenAlexW3110998061

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.