Evidence map›Paper›PMID 21653634›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Activation of P2Y1 and P2Y2 receptors induces chloride secretion via calcium-activated chloride channels in kidney inner medullary collecting duct cells.

Madhumitha Rajagopal, Paru P Kathpalia, Sheela V Thomas, Alan C Pao

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

  1. Purinergic Receptor P2Y2 Regulates Neurogenesis and Functional Recovery Following Spinal Cord Injury in Zebrafish.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. Chloride secretion by renal collecting ducts.Current opinion in nephrology and hypertension · 2015
    Article
  12. Harvest and primary culture of the murine aldosterone-sensitive distal nephron.American journal of physiology. Renal physiology · 2015
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

4 authors at 1 institution in 1 country.

Madhumitha RajagopalDiv. of Nephrology, Dept. of Medicine, Stanford Univ., CA 94304, USA.
Paru P Kathpalia
Sheela V Thomas
Alan C Pao
Stanford University · US

Funding

TRAINING PROGRAM IN ACADEMIC NEPHROLOGYT32DK007357 · NIDDK · STANFORD UNIVERSITY · PI CHERTOW, GLENN MATTHEW · 1986 to 2022
$4.8M
The Functional Role of the PXL Domain of SGK1 in Epithelial Sodium TransportK08DK073487 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI PAO, ALAN C · 2006 to 2010
$599k
NIDDK NIH HHS K08 DK073487NIDDK NIH HHS K08-DK-073487NIDDK NIH HHS T32 DK007357NIDDK NIH HHS T32-DK07357-26A1
6 · The paper itself

Abstract

Dysregulation of urinary sodium chloride (NaCl) excretion can result in extracellular fluid (ECF) volume expansion and hypertension. Recent studies demonstrated that urinary nucleotide excretion increases in mice ingesting a high-salt diet and that these increases in extracellular nucleotides can signal through P2Y(2) receptors in the kidney collecting duct to inhibit epithelial Na(+) channels (ENaC). However, under conditions of ECF volume expansion brought about by high-dietary salt intake, ENaC activity should already be suppressed. We hypothesized that alternative pathways exist by which extracellular nucleotides control renal NaCl excretion. We used an inner medullary collecting duct (mIMCD-K2) cell line in an Ussing chamber system as a model to study additional ion transport pathways that are regulated by extracellular nucleotides. When ENaC was inhibited, the addition of adenosine triphosphate (ATP) to the basal side of cell sheets activated both P2Y(1) and P2Y(2) receptors, inducing a transient increase in short-circuit current (I(sc)); addition of ATP to the apical side activated only P2Y(2) receptors, inducing first a transient and then a sustained increase in I(sc). The ATP-induced increases in I(sc) were blocked by pretreatment with a phospholipase C (PLC) inhibitor, a calcium (Ca(2+)) chelator, or Ca(2+)-activated Cl(-) channel (CACC) inhibitors, suggesting that ATP signals through both PLC and intracellular Ca(2+) to activate CACC. We propose that P2Y(1) and P2Y(2) receptors operate in tandem in IMCD cells to provide an adaptive mechanism for enhancing urinary NaCl excretion in the setting of high-dietary NaCl intake.

Indexed as

Adenosine TriphosphateAnimalsBiological TransportCalciumCell LineChloride ChannelsChloridesIon TransportKidney Tubules, CollectingMiceModels, AnimalReceptors, Purinergic P2Y1Receptors, Purinergic P2Y2Signal TransductionSodium ChlorideSodium Chloride, DietaryAdenosine TriphosphateCalciumChloride ChannelsChloridesReceptors, Purinergic P2Y1Receptors, Purinergic P2Y2Sodium ChlorideSodium Chloride, DietaryType C Phospholipases

Identifiers

PMID21653634
PMCPMC3174549
OpenAlexW2148195018

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.