Evidence map›Paper›PMID 27053687›Full record

ArticleAmerican journal of physiology. Renal physiology2016

Renal tubular epithelial cell prorenin receptor regulates blood pressure and sodium transport.

Nirupama Ramkumar, Deborah Stuart, Elena Mironova, Vladislav Bugay, Shuping Wang, Nikita Abraham, Atsuhiro Ichihara, James D Stockand, Donald E Kohan

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Renal tubular (pro)renin receptor deletion exacerbates kidney injury inAmerican journal of physiology. Renal physiology · 2025
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Review
  15. Article
  16. Soluble (Pro)Renin Receptor as a Negative Regulator of NCC (NaHypertension (Dallas, Tex. : 1979) · 2021
    Article
  17. Review
  18. Article
  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

9 authors at 3 institutions in 2 countries.

Nirupama RamkumarDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah; nirupama.ramkumar@hsc.utah.edu.
Deborah StuartDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah;
Elena MironovaDepartment of Physiology, University of Texas Health Science Center, San Antonio, Texas; and.
Vladislav BugayDepartment of Physiology, University of Texas Health Science Center, San Antonio, Texas; and.
Shuping WangDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah;
Nikita AbrahamDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah;
Atsuhiro IchiharaDepartment of Medicine II, Endocrinology and Hypertension, Tokyo Women's Medical University, Tokyo, Japan.
James D StockandDepartment of Physiology, University of Texas Health Science Center, San Antonio, Texas; and.
Donald E KohanDivision of Nephrology and Hypertension, University of Utah Health Sciences Center, Salt Lake City, Utah; Veterans Affairs Medical Center, Salt Lake City, Utah;
University of Utah · USThe University of Texas Health Science Center at San Antonio · USTokyo Women's Medical University · JP

Funding

Regulation of renal Na+ excretion by antidiuretic hormoneF32DK104572 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MIRONOVA, ELENA · 2014 to 2017
$195k
Collecting duct renin regulation of blood pressure in health and hypertensionI01BX002510 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI KOHAN, DONALD E · 2015 to 2018
–
BLRD VA I01 BX002510NIDDK NIH HHS F32 DK104572
6 · The paper itself

Abstract

The physiological significance of the renal tubular prorenin receptor (PRR) has been difficult to elucidate due to developmental abnormalities associated with global or renal-specific PRR knockout (KO). We recently developed an inducible renal tubule-wide PRR KO using the Pax8/LC1 transgenes and demonstrated that disruption of renal tubular PRR at 1 mo of age caused no renal histological abnormalities. Here, we examined the role of renal tubular PRR in blood pressure (BP) regulation and Na(+) excretion and investigated the signaling mechanisms by which PRR regulates Na(+) balance. No detectable differences in BP were observed between control and PRR KO mice fed normal- or low-Na(+) diets. However, compared with controls, PRR KO mice had elevated plasma renin concentration and lower cumulative Na(+) balance with normal- and low-Na(+) intake. PRR KO mice had an attenuated hypertensive response and reduced Na(+) retention following angiotensin II (ANG II) infusion. Furthermore, PRR KO mice had significantly lower epithelial Na(+) channel (ENaC-α) expression. Treatment with mouse prorenin increased, while PRR antagonism decreased, ENaC activity in isolated split-open collecting ducts (CD). The prorenin effect was prevented by protein kinase A and Akt inhibition, but unaffected by blockade of AT1, ERK1/2, or p38 MAPK pathways. Taken together, these data indicate that renal tubular PRR, likely via direct prorenin/renin stimulation of PKA/Akt-dependent pathways, stimulates CD ENaC activity. Absence of renal tubular PRR promotes Na(+) wasting and reduces the hypertensive response to ANG II.

Indexed as

Angiotensin IIAnimalsBlood PressureCyclic AMP-Dependent Protein KinasesDiet, Sodium-RestrictedEpithelial CellsEpithelial Sodium ChannelsKidney TubulesKidney Tubules, CollectingMaleMAP Kinase Signaling SystemMiceMice, KnockoutOncogene Protein v-aktProrenin ReceptorReceptors, Cell SurfaceAngiotensin IICyclic AMP-Dependent Protein KinasesEpithelial Sodium ChannelsOncogene Protein v-aktProrenin ReceptorReceptors, Cell SurfaceSodiumSodium, Dietaryangiotensin IIblood pressureprorenin receptorsodium transport

Identifiers

PMID27053687
PMCPMC4967157
OpenAlexW2317924481

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.