Evidence map›Paper›PMID 19407217›Full record

ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009

Regulation of colonic apical potassium (BK) channels by cAMP and somatostatin.

M D Perry, G I Sandle

Abstract read
In one paragraph

Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

  1. Pooled it
  2. Ion transport and epithelial barrier dysfunction in experimental models of ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2025
    Review
  3. Article
  4. Somatostatin peptides prevent increased human colonic epithelial permeability induced by hypoxia.American journal of physiology. Gastrointestinal and liver physiology · 2024
    Article
  5. Review
  6. Review
  7. Is intestinal transport dysfunctional in COVID-19-related diarrhea?American journal of physiology. Gastrointestinal and liver physiology · 2023
    Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Colonic potassium handling.Pflugers Archiv : European journal of physiology · 2010
    Review
  15. Cholesterol and ion channels.Sub-cellular biochemistry · 2010
    Review
  16. 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

2 authors at 1 institution in 1 country.

M D PerryInstitute of Molecular Medicine, St James's University Hospital, Leeds LS9 7TF, United Kingdom.
G I Sandle
St James's University Hospital · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

High-conductance apical K+ (BK) channels are present in surface colonocytes of mammalian (including human) colon. Their location makes them well fitted to contribute to the excessive intestinal K(+) losses often associated with infective diarrhea. Since many channel proteins are regulated by phosphorylation, we evaluated the roles of protein kinase A (PKA) and phosphatases in the modulation of apical BK channel activity in surface colonocytes from rat distal colon using patch-clamp techniques, having first increased channel abundance by chronic dietary K+ enrichment. We found that PKA activation using 50 micromol/l forskolin and 5 mmol/l 3-isobutyl-1-methylxanthine stimulated BK channels in cell-attached patches and the catalytic subunit of PKA (200 U/ml) had a similar effect in excised inside-out patches. The antidiarrheal peptide somatostatin (SOM; 2 micromol/l) had a G protein-dependent inhibitory effect on BK channels in cell-attached patches, which was unaffected by pretreatment with 10 micromol/l okadaic acid (an inhibitor of protein phosphatase type 1 and type 2A) but completely prevented by pretreatment with 100 micromol/l Na+ orthovanadate and 10 micromol/l BpV (inhibitors of phosphoprotein tyrosine phosphatase). SOM also inhibited apical BK channels in surface colonocytes in human distal colon. We conclude that cAMP-dependent PKA activates apical BK channels and may enhance colonic K+ losses in some cases of secretory diarrhea. SOM inhibits apical BK channels through a phosphoprotein tyrosine phosphatase-dependent mechanism, which could form the basis of new antidiarrheal strategies.

Indexed as

Ion Channel GatingProtein Processing, Post-TranslationalAnimalsCatalytic DomainCell PolarityColonCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme ActivationEnzyme ActivatorsEnzyme InhibitorsHumansIntestinal MucosaIn Vitro TechniquesKineticsLarge-Conductance Calcium-Activated Potassium ChannelsCyclic AMPCyclic AMP-Dependent Protein KinasesEnzyme ActivatorsEnzyme InhibitorsLarge-Conductance Calcium-Activated Potassium ChannelsPhosphoprotein PhosphatasesPotassiumPotassium, DietaryProtein Tyrosine PhosphatasesSomatostatin

Identifiers

PMID19407217
PMCPMC2711756
OpenAlexW2167146128

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.