Evidence map›Paper›PMID 23739592›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Attenuation of lithium-induced natriuresis and kaliuresis in P2Y₂ receptor knockout mice.

Yue Zhang, Lijun Li, Donald E Kohan, Carolyn M Ecelbarger, Bellamkonda K Kishore

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. ATP release into ADPKD cysts via pannexin-1/P2X7 channels decreases ENaC activity.Biochemical and biophysical research communications · 2019
    Article
  4. Article
  5. Article
  6. Genetic Deletion of P2YFrontiers in physiology · 2018
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
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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

5 authors at 3 institutions in 1 country.

Yue ZhangNephrology Research, Department of Veterans Administration Salt Lake City Health Care System, Salt Lake City, UT 84148, USA.
Lijun Li
Donald E Kohan
Carolyn M Ecelbarger
Bellamkonda K Kishore
University of Utah · USGeorgetown University · USIndividual Differences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Whole body knockout (KO) of the P2Y₂ receptor (P2Y₂R) results in enhanced vasopressin V2 receptor activity and increased renal Na⁺ conservation. We hypothesized that P2Y₂R KO mice would be less sensitive to lithium-induced natriuresis and kaliuresis due to attenuated downregulation of one or more of the major renal Na⁺ or K⁺ transporter/channel proteins. KO and wild-type (WT) mice were fed a control or lithium-added diet (40 mmol/kg food) for 14 days. Lithium-induced natriuresis and kaliuresis were significantly (~25%) attenuated in KO mice. The subunits of the epithelial Na⁺ channel (ENaC) were variably affected by lithium and genotype, but, overall, medullary levels were decreased substantially by lithium (15-60%) in both genotypes. In contrast, cortical, β-, and γ-ENaC were increased by lithium (~50%), but only in WT mice. Moreover, an assessment of ENaC activity by benzamil sensitivity suggested that lithium increased ENaC activity in WT mice but in not KO mice. In contrast, medullary levels of Na⁺-K⁺-2Cl⁻ cotransporter 2 and cortical levels of the renal outer medullary K⁺ channel were not downregulated by lithium and were significantly (15-76%) higher in KO mice under both dietary conditions. In addition, under control conditions, tissue osmolality of the inner medulla as well as furosemide sensitivity were significantly higher in KO mice versus WT mice. Therefore, we suggest that increased expression of these proteins, particularly in the control state, reduces Na⁺ delivery to the distal nephron and provides a buffer to attenuate collecting duct-mediated natriuresis and kaliuresis. Additional studies are warranted to explore the potential therapeutic benefits of purinergic antagonism.

Indexed as

AldosteroneAnalysis of VarianceAnimalsDietDiureticsEpithelial Sodium ChannelsGenotypeKidneyKidney MedullaKidney Tubules, CollectingLithiumMiceMice, KnockoutNatriuresisNephronsOsmolar ConcentrationAldosteroneDiureticsEpithelial Sodium ChannelsLithiumPotassiumReceptors, Purinergic P2Y2Slc12a1 protein, mouseSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 1aldosteroneATPepithelial sodium channelnephrogenic diabetes insipiduspotassium channelssodium transportersvasopressin

Identifiers

PMID23739592
PMCPMC4596727
OpenAlexW2066186494

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.