Evidence map›Paper›PMID 10919872›Full record

ArticleThe Journal of general physiology2000

Extracellular ATP inhibits the small-conductance K channel on the apical membrane of the cortical collecting duct from mouse kidney.

M Lu, G G MacGregor, W Wang, G Giebisch

Open access · greenAbstract read
In one paragraph

Article in The Journal of general physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Epithelial transport inThe Journal of general physiology · 2017
    Review
  3. Large-conductance CaThe Journal of physiology · 2017
    Article
  4. Article
  5. Article
  6. Collecting duct principal cell transport processes and their regulation.Clinical journal of the American Society of Nephrology : CJASN · 2015
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. P2Y receptors and kidney function.Wiley interdisciplinary reviews. Membrane transport and signaling · 2012
    Article
  13. Regulation of renal NaCl and water transport by the ATP/UTP/P2Y2 receptor system.American journal of physiology. Renal physiology · 2011
    Review
  14. Coupled ATP and potassium efflux from intercalated cells.American journal of physiology. Renal physiology · 2011
    Article
  15. Article
  16. Dietary Na+ inhibits the open probability of the epithelial sodium channel in the kidney by enhancing apical P2Y2-receptor tone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010
    Article
  17. Article
  18. Article
  19. Connexin 30 deficiency impairs renal tubular ATP release and pressure natriuresis.Journal of the American Society of Nephrology : JASN · 2009
    Article
  20. Homeostatic synapse-driven membrane plasticity in nucleus accumbens neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    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 2 institutions in 1 country.

M LuDepartment of Cellular & Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.
G G MacGregor
W Wang
G Giebisch
Yale University · USNew York Medical College · US

Funding

MODULATION OF K+ CHANNELS IN RENAL COLLECTING DUCTR01DK047402 · NIDDK · NEW YORK MEDICAL COLLEGE · PI WANG, WENHUI · 1999 to 2007
$2.3M
ROMK CHANNEL FUNCTION AND REGULATION IN KIDNEYR01DK054998 · NIDDK · YALE UNIVERSITY · PI GIEBISCH, GERHARD H · 1999 to 2003
$883k
MODULATION OF K+ CHANNELS IN RENAL COLLECTING DUCTR29DK047402 · NIDDK · NEW YORK MEDICAL COLLEGE · PI WANG, WEN-HUI · 1994 to 1998
–
NIDDK NIH HHS DK 47402NIDDK NIH HHS DK 54998NIDDK NIH HHS R01 DK047402NIDDK NIH HHS R01 DK054998
6 · The paper itself

Abstract

We have used the patch-clamp technique to study the effects of changing extracellular ATP concentration on the activity of the small-conductance potassium channel (SK) on the apical membrane of the mouse cortical collecting duct. In cell-attached patches, the channel conductance and kinetics were similar to its rat homologue. Addition of ATP to the bathing solution of split-open single cortical collecting ducts inhibited SK activity. The inhibition of the channel by ATP was reversible, concentration dependent (K(i) = 64 microM), and could be completely prevented by pretreatment with suramin, a specific purinergic receptor (P(2)) blocker. Ranking of the inhibitory potency of several nucleotides showed strong inhibition by ATP, UTP, and ATP-gamma-S, whereas alpha, beta-Me ATP, and 2-Mes ATP failed to affect channel activity. This nucleotide sensitivity is consistent with P(2)Y(2) purinergic receptors mediating the inhibition of SK by ATP. Single channel analysis further demonstrated that the inhibitory effects of ATP could be elicited through activation of apical receptors. Moreover, the observation that fluoride mimicked the inhibitory action of ATP suggests the activation of G proteins during purinergic receptor stimulation. Channel inhibition by ATP was not affected by blocking phospholipase C and protein kinase C. However, whereas cAMP prevented channel blocking by ATP, blocking protein kinase A failed to abolish the inhibitory effects of ATP. The reduction of K channel activity by ATP could be prevented by okadaic acid, an inhibitor of protein phosphatases, and KT5823, an agent that blocks protein kinase G. Moreover, the effect of ATP was mimicked by cGMP and blocked by L-NAME (N(G)-nitro-l-arginine methyl ester). We conclude that the inhibitory effect of ATP on the apical K channel is mediated by stimulation of P(2)Y(2) receptors and results from increasing dephosphorylation by enhancing PKG-sensitive phosphatase activity.

Indexed as

CarbazolesIndolesPotassium Channels, Calcium-ActivatedAdenosine TriphosphateAffinity LabelsAlkaloidsAnimalsColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsExtracellular SpaceIon Channel GatingKidney Tubules, CollectingMembrane Potentials2-methylthio-ATPadenosine 5'-O-(3-thiotriphosphate)Adenosine TriphosphateAffinity LabelsAlkaloidsalpha,beta-methyleneadenosine 5'-triphosphatecalphostin CCarbazolesColforsinCyclic AMPCyclic AMP-Dependent Protein KinasesCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsIndolesKT 5823NaphthalenesNG-Nitroarginine Methyl EsterOkadaic AcidPhosphoprotein PhosphatasesPotassiumPotassium ChannelsPotassium Channels, Calcium-ActivatedProtein KinasesReceptors, PurinergicSmall-Conductance Calcium-Activated Potassium ChannelsThionucleotidesUridine Triphosphate

Identifiers

PMID10919872
PMCPMC2229488
OpenAlexW2079773628

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.