Evidence map›Paper›PMID 25587122›Full record

ArticleAmerican journal of physiology. Renal physiology2015

Flow regulation of endothelin-1 production in the inner medullary collecting duct.

Meghana M Pandit, Edward W Inscho, Shali Zhang, Tsugio Seki, Rajeev Rohatgi, Luca Gusella, Bellamkonda Kishore, Donald E Kohan

Open access · greenAbstract 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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
4.0field-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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
  2. Review
  3. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  4. Article
  5. Review
  6. Review
  7. Greater natriuretic response to ENaC inhibition in male versus female Sprague-Dawley rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Cellular cholesterol modifies flow-mediated gene expression.American journal of physiology. Renal physiology · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Interplay between renal endothelin and purinergic signaling systems.American journal of physiology. Renal physiology · 2017
    Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 1 country.

Meghana M PanditDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah; Department of Pharmaceutics and Pharmaceutical Chemistry, Salt Lake City, Utah;
Edward W InschoUniversity of Alabama at Birmingham, Birmingham, Alabama;
Shali ZhangUniversity of Alabama at Birmingham, Birmingham, Alabama;
Tsugio SekiDepartment of Medical Education, California Northstate University, Elk Grove, California;
Rajeev RohatgiDepartment of Medicine, James J. Peter Veterans Affairs Medical Center, Bronx, New York; Department of Medicine and Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York; and.
Luca GusellaDepartment of Medicine, James J. Peter Veterans Affairs Medical Center, Bronx, New York; Department of Medicine and Pediatrics, Icahn School of Medicine at Mount Sinai, New York, New York; and.
Bellamkonda KishoreDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah; Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah.
Donald E KohanDivision of Nephrology, University of Utah Health Sciences Center, Salt Lake City, Utah; Department of Pharmaceutics and Pharmaceutical Chemistry, Salt Lake City, Utah; Salt Lake Veterans Affairs Medical Center, Salt Lake City, Utah donald.kohan@hsc.utah.edu.
University of Utah · USUniversity of Alabama at Birmingham · USCalifornia Northstate University · USIcahn School of Medicine at Mount Sinai · USJames J. Peters VA Medical Center · US

Funding

Renal endothelin receptor-specific function in angiotensin ll-dependent hypertensP01HL095499 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SULLIVAN, JENNIFER C · 2010 to 2014
$11.1M
TLR4 in the Regulation of Renal Microvascular FunctionR01DK044628 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI INSCHO, EDWARD W · 2000 to 2021
$6.2M
The Inflammatory Cytokines, MCP-1 and TGF-Beta, Mediate Renal Autoregulatory ImpaR01HL098135 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI INSCHO, EDWARD W · 2010 to 2014
$1.8M
Targeting Renal Purinergic Signaling for the Treatment of Lithium-induced NDII01BX000596 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI KISHORE, BELLAMKONDA K · 2011 to 2019
–
PURINERGIC REGULATION OF THE RENAL MICROVASCULATURER29DK044628 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI INSCHO, EDWARD W. · 1994 to 1998
–
BLRD VA I01 BX000596NHLBI NIH HHS HL-098135NHLBI NIH HHS P01-HL-095499NIDDK NIH HHS DK-044628
6 · The paper itself

Abstract

Collecting duct-derived endothelin (ET)-1 is an autocrine inhibitor of Na(+) and water reabsorption; its deficiency causes hypertension and water retention. Extracellular fluid volume expansion increases collecting duct ET-1, thereby promoting natriuresis and diuresis; however, how this coupling between volume expansion and collecting duct ET-1 occurs is incompletely understood. One possibility is that volume expansion increases tubular fluid flow. To investigate this, cultured IMCD3 cells were subjected to static or flow conditions. Exposure to a shear stress of 2 dyn/cm(2) for 2 h increased ET-1 mRNA content by ∼2.3-fold. Absence of perfusate Ca(2+), chelation of intracellular Ca(2+), or inhibition of Ca(2+) signaling (calmodulin, Ca(2+)/calmodulin-dependent kinase, calcineurin, PKC, or phospholipase C) prevented the flow response. Evaluation of possible flow-activated Ca(2+) entry pathways revealed no role for transient receptor potential (TRP)C3, TRPC6, and TRPV4; however, cells with TRPP2 (polycystin-2) knockdown had no ET-1 flow response. Flow increased intracellular Ca(2+) was blunted in TRPP2 knockdown cells. Nonspecific blockade of P2 receptors, as well as specific inhibition of P2X7 and P2Y2 receptors, prevented the ET-1 flow response. The ET-1 flow response was not affected by inhibition of either epithelial Na(+) channels or the mitochondrial Na(+)/Ca(2+) exchanger. Taken together, these findings provide evidence that in IMCD3 cells, flow, via polycystin-2 and P2 receptors, engages Ca(2+)-dependent signaling pathways that stimulate ET-1 synthesis.

Indexed as

AnimalsCalciumCalcium SignalingCell LineDiuresisEndothelin-1Epithelial Sodium ChannelsKidney MedullaKidney Tubules, CollectingMaleMiceNatriuresisRats, Sprague-DawleyReceptors, PurinergicRNA, MessengerSodiumCalciumEndothelin-1Epithelial Sodium ChannelsReceptors, PurinergicRNA, MessengerSodiumTransient Receptor Potential ChannelsTRPP Cation ChannelsWatercollecting ductendothelinflowpurinergic

Identifiers

PMID25587122
PMCPMC4360032
OpenAlexW2002632263

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.