Evidence map›Paper›PMID 20616305›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2010

Mucosal potassium efflux mediated via Kcnn4 channels provides the driving force for electrogenic anion secretion in colon.

N S Nanda Kumar, Satish K Singh, Vazhaikkurichi M Rajendran

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 37 citations in OpenAlex.

  1. Role of ion channels in gastrointestinal cancer.World journal of gastroenterology · 2019
    Review
  2. Review
  3. Dextran sulfate sodium-induced chronic colitis attenuates CaAmerican journal of physiology. Cell physiology · 2018
    Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Article
  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. Review
  15. Article
  16. Physiology of epithelial chloride and fluid secretion.Cold Spring Harbor perspectives in medicine · 2012
    Article
  17. Article
  18. Non-systemic drugs: a critical review.Current pharmaceutical design · 2012
    Review
  19. Characteristics of Kcnn4 channels in the apical membranes of an intestinal epithelial cell line.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
  20. 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

3 authors at 2 institutions in 1 country.

N S Nanda KumarDepts. of Biochemistry and Microbiology, West Virginia Univ. School of Medicine, Morgantown, 26506, USA.
Satish K Singh
Vazhaikkurichi M Rajendran
VA Boston Healthcare System · USWest Virginia University · US

Funding

Role of IK channels in rat distal colonR01DK018777 · NIDDK · YALE UNIVERSITY · PI RAJENDRAN, VAZHAIKKURICHI M. · 1986 to 2010
$2.5M
NIDDK NIH HHS DK-018777NIDDK NIH HHS R01 DK018777
6 · The paper itself

Abstract

Intermediate conductance K(+) (Kcnn4) channels are present in both mucosal and serosal membranes of colon. However, only serosal Kcnn4 channels have been shown to be essential for agonist-induced (cAMP and Ca(2+)) anion secretion. The present study sought to determine whether mucosal Kcnn4 channels also play a role in colonic anion secretion. Mucosal-to-serosal and serosal-to-mucosal unidirectional (86)Rb (K(+) surrogate) fluxes as well as short-circuit current (I(sc); a measure of anion secretion) were measured under voltage-clamp conditions in distal colon from rats fed either a standard or K(+)-free diet. 5,6-Dichloro-1-ethyl-1,3-dihydro-2H-benzimidazole-2-one (DC-EBIO) was used to activate Kcnn4 channels. Mucosal DC-EBIO both induced K(+) secretion and enhanced anion secretion in normal rat distal colon. The DC-EBIO-induced K(+) secretion was completely blocked by nonspecific (Ba(2+)) and Kcnn4-specific (TRAM-34) inhibitors, but was not blocked by the large-conductance K(+) (iberiotoxin), small-conductance K(+) (apamin), or KCNQ1 (chromanol 293B) specific blockers. Ba(2+) and TRAM-34 also inhibited DC-EBIO-enhanced anion secretion. The DC-EBIO-enhanced anion secretion was completely inhibited by the nonspecific anion channel blocker 5-nitro-2-(3-phenylpropyl-amino)benzoic acid, whereas it was only partially inhibited by CFTR [CFTR(inh)-172, glibenclamide]- and CaCC (niflumic acid)-specific Cl(-) channel blockers. In contrast, mucosal DC-EBIO-enhanced K(+) and anion secretion was not present in distal colon of dietary K-depleted rats, indicating absence of mucosal Kcnn4 channels. These observations indicate that mucosal Kcnn4 channels are capable of driving agonist-induced anion secretion mediated via CFTR and CaCC and likely contribute to stool K(+) losses that accompany diarrheal illnesses.

Indexed as

AnimalsAnionsBenzimidazolesChloride ChannelsColonCystic Fibrosis Transmembrane Conductance RegulatorElectric ImpedanceIntermediate-Conductance Calcium-Activated Potassium ChannelsIntestinal MucosaMalePotassiumRatsRats, Sprague-Dawley5,6-dichloro-1-ethyl-1,3-dihydro-2H-benzimidazol-2-oneAnionsBenzimidazolesChloride ChannelsClca5 protein, ratCystic Fibrosis Transmembrane Conductance RegulatorIntermediate-Conductance Calcium-Activated Potassium ChannelsKcnn4 protein, ratPotassium

Identifiers

PMID20616305
PMCPMC2950693
OpenAlexW2164015725

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.