Evidence map›Paper›PMID 21169331›Full record

ArticleExperimental physiology2011

Activation of the basolateral membrane Cl- conductance essential for electrogenic K+ secretion suppresses electrogenic Cl- secretion.

Quanhua He, Susan T Halm, Jin Zhang, Dan R Halm

Open access · bronzeAbstract read
In one paragraph

Article in Experimental physiology, 2011. 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
0.9field-weighted citation impact, top 27% 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, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Anoctamin Channels in Human Myometrium: A Novel Target for Tocolysis.Reproductive sciences (Thousand Oaks, Calif.) · 2018
    Article
  9. Ion channels in regulated cell death.Cellular and molecular life sciences : CMLS · 2016
    Review
  10. Article
  11. Article
  12. Article
  13. Role of the BK channel (KCa1.1) during activation of electrogenic K+ secretion in guinea pig distal colon.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  14. Article
  15. Article
  16. Anoctamins.Pflugers Archiv : European journal of physiology · 2011
    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

4 authors at 1 institution in 1 country.

Quanhua HeDepartment of Neuroscience, Cell Biology & Physiology, Wright State University Boonshoft School of Medicine, 3640 Colonel Glenn Highway, Dayton, OH 45435, USA.
Susan T Halm
Jin Zhang
Dan R Halm
Wright State University · US

Funding

Regulation of Secretory Ion Channels in Colonic CryptsR01DK065845 · NIDDK · WRIGHT STATE UNIVERSITY · PI HALM, DAN R · 2005 to 2009
$1.3M
NIDDK NIH HHS DK65845NIDDK NIH HHS R01 DK065845
6 · The paper itself

Abstract

Adrenaline activates transient Cl(-) secretion and sustained K(+) secretion across isolated distal colonic mucosa of guinea-pigs. The Ca(2+)-activated Cl(-) channel inhibitor CaCCinh-A01 (30 μm) significantly reduced electrogenic K(+) secretion, detected as short-circuit current (I(sc)). This inhibition supported the cell model for K(+) secretion in which basolateral membrane Cl(-) channels provide an exit pathway for Cl(-) entering the cell via Na(+)-K(+)-2Cl(-) cotransporters. CaCCinh-A01 inhibited both I(sc) and transepithelial conductance in a concentration-dependent manner (IC(50) = 6.3 μm). Another Cl(-) channel inhibitor, GlyH-101, also reduced sustained adrenaline-activated I(sc) (IC(50) = 9.4 μm). Adrenaline activated whole-cell Cl(-) current in isolated intact colonic crypts, confirmed by ion substitution. This adrenaline-activated whole-cell Cl(-) current was also inhibited by CaCCinh-A01 or GlyH-101. In contrast to K(+) secretion, CaCCinh-A01 augmented the electrogenic Cl(-) secretion activated by adrenaline as well as that activated by prostaglandin E(2). Synergistic Cl(-) secretion activated by cholinergic/prostaglandin E(2) stimulation was insensitive to CaCCinh-A01. Colonic expression of the Ca(2+)-activated Cl(-) channel protein Tmem16A was supported by RT-PCR detection of Tmem16A mRNA, by immunoblot with a Tmem16A antibody, and by detection of immunofluorescence in lateral membranes of epithelial cells. Alternative splices of Tmem16A were detected for exons that are involved in channel activation. Inhibition of K(+) secretion and augmentation of Cl(-) secretion by CaCCinh-A01 support a common colonic cell model for these two ion secretory processes, such that activation of basolateral membrane Cl(-) channels contributes to the production of electrogenic K(+) secretion and limits the rate of Cl(-) secretion. Maximal physiological Cl(-) secretion occurs only for synergistic activation mechanisms that close these basolateral membrane Cl(-) channels.

Indexed as

AnimalsCell MembraneChloride ChannelsChloridesCholinergic AgentsColonDinoprostoneEpinephrineEpithelial CellsGlycineGuinea PigsHydrazinesIntestinal MucosaMaleMembrane PotentialsMembrane ProteinsChloride ChannelsChloridesCholinergic AgentsDinoprostoneEpinephrineGlycineHydrazinesMembrane ProteinsN-(2-naphthalenyl)-((3,5-dibromo-2,4-dihydroxyphenyl)methylene)glycine hydrazidePotassiumSodium-Potassium-Chloride Symporters

Identifiers

PMID21169331
PMCPMC3041851
OpenAlexW1518251966

What OpenQuestion holds

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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.