Evidence map›Paper›PMID 23145369›Full record

ArticleWiley interdisciplinary reviews. Membrane transport and signaling2012

P2Y receptors and kidney function.

Volker Vallon, James Stockand, Timo Rieg

Abstract read
In one paragraph

Article in Wiley interdisciplinary reviews. Membrane transport and signaling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

23 citing papers in PubMed, 88 citations in OpenAlex.

  1. Novel Roles of GPCRs in the Renal Collecting Duct.Physiology (Bethesda, Md.) · 2026
    Review
  2. GPER1 activation regulates renal purinergic P2YAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Knockout ofAmerican journal of physiology. Renal physiology · 2019
    Article
  14. Renal NaAmerican journal of physiology. Renal physiology · 2019
    Article
  15. Article
  16. Article
  17. Interplay between renal endothelin and purinergic signaling systems.American journal of physiology. Renal physiology · 2017
    Review
  18. Review
  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

3 authors at 2 institutions in 1 country.

Volker VallonDepartment of Medicine, University of California San Diego, San Diego, CA 92161, USA; VA San Diego Healthcare System, San Diego California, San Diego, CA 92161, USA; Department of Pharmacology, University of California San Diego, La Jolla, CA 92093, USA.
James Stockand
Timo Rieg
VA San Diego Healthcare System · USThe University of Texas Health Science Center at San Antonio · US

Funding

UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
GLOMERULAR AND TUBULAR FUNCTION IN THE DIABETIC KIDNEYR01DK056248 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI THOMSON, SCOTT CULVER · 1999 to 2014
$4.6M
AUTOREGULATION OF GLOMERULAR FILTRATION RATER01DK028602 · NIDDK · VETERANS MEDICAL RESEARCH FDN/SAN DIEGO · PI BLANTZ, ROLAND C · 1986 to 2011
$3.9M
Adrenergic and Purinergic Regulation of Target CellsR01GM066232 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI INSEL, PAUL A · 2004 to 2010
$1.9M
Blood Pressure Regulation by OAT3R01HL094728 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI ERALY, SATISH A, VALLON, VOLKER · 2010 to 2014
$1.9M
Regulation of renal Na handling in the collecting duct by local purinergic toneR01DK087460 · NIDDK · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI STOCKAND, JAMES D · 2010 to 2013
$1.3M
NHLBI NIH HHS R01 HL094728NIDDK NIH HHS P30 DK079337NIDDK NIH HHS R01 DK028602NIDDK NIH HHS R01 DK056248NIDDK NIH HHS R01 DK087460NIGMS NIH HHS R01 GM066232
6 · The paper itself

Abstract

Cellular release of nucleotides is of physiological importance to regulate and maintain cell function and integrity. Also in the tubular and collecting duct system of the kidney, nucleotides are released in response to changes in cell volume or luminal flow rate and act in a paracrine and autocrine way on basolateral and luminal P2Y receptors. Recent studies using gene knockout mice assigned a prominent role to G protein-coupled P2Y(2) receptors, which are activated by both ATP and UTP. The antidiuretic hormone, arginine-vasopressin (AVP), and possibly an increase in collecting duct cell volume induce ATP release. The subsequent activation of P2Y(2) receptors inhibits AVP-induced cAMP formation and water reabsorption, which stabilizes cell volume and facilitates water excretion. An increase in NaCl intake enhances luminal release of ATP and UTP in the aldosterone-sensitive distal nephron which by activating apical P2Y(2) receptors and phospholipase C lowers the open probability of the epithelial sodium channel ENaC, thereby facilitating sodium excretion. Thus, the renal ATP/UTP/P2Y(2) receptor system not only serves to preserve cell volume and integrity but is also regulated by stimuli that derive from body NaCl homeostasis. The system also inhibits ENaC activity during aldosterone escape, i.e. when sodium reabsorption via ENaC is inappropriately high. The P2Y(2) receptor tone inhibits the expression and activity of the Na-K-2Cl cotransporter NKCC2 in the thick ascending limb and mediates vasodilation. While the role of other P2Y receptors in the kidney is less clear, the ATP/UTP/P2Y(2) receptor system regulates NaCl and water homeostasis and blood pressure.

Identifiers

PMID23145369
PMCPMC3490424
OpenAlexW2087328390

What OpenQuestion holds

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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 OpenQuestion graph.