Evidence map›Paper›PMID 10482912›Full record

ArticleBritish journal of pharmacology1999

Effects of anion channel antagonists in canine colonic myocytes: comparative pharmacology of Cl-, Ca2+ and K+ currents.

G M Dick, I D Kong, K M Sanders

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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

22 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Ano1 as a regulator of proliferation.American journal of physiology. Gastrointestinal and liver physiology · 2011
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Ca2+-activated Cl- current in retinal arteriolar smooth muscle.Investigative ophthalmology & visual science · 2009
    Article
  14. Inhibition of a cardiac sarcoplasmic reticulum chloride channel by tamoxifen.Pflugers Archiv : European journal of physiology · 2008
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. ClNetherlands heart journal : monthly journal of the Netherlands Society of Cardiology and the Netherlands Heart Foundation · 2001
    Review
  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 1 institution in 1 country.

G M DickDepartment of Physiology & Cell Biology, University of Nevada School of Medicine, Anderson Medical Building/352, Reno, Nevada, NV 89557, USA.
I D Kong
K M Sanders
University of Nevada, Reno · US

Funding

Tissue, Cell and Tissue Culture CoreP01DK041315 · NIDDK · UNIVERSITY OF NEVADA RENO · PI WARD, SEAN M · 1989 to 2018
$26.3M
NIDDK NIH HHS DK41315NIDDK NIH HHS P01 DK041315
6 · The paper itself

Abstract

1. Volume-Sensitive, Outwardly Rectifying (VSOR) Cl- currents were measured in canine colonic myocytes by whole-cell patch clamp. Decreasing extracellular osmolarity 50 milliosmoles l-1 activated current that was carried by Cl- and 5 - 7 times greater in the outward direction. 2. Niflumic acid, an inhibitor of Ca2+-activated Cl- channels, did not inhibit VSOR Cl- current. Glibenclamide, an antagonist of CFTR, and anthracene-9-carboxylate (9-AC) inhibited current less than 25% at 100 microM. 3. DIDS (4, 4-diisothiocyanato-stilbene-2,2'disulphonate) inhibited VSOR Cl- current more potently than SITS (4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulphonate). IC50s were 0.84 and 226 microM, respectively. 4. VSOR Cl- current was strongly inhibited by tamoxifen ([Z]-1-[p-dimethylaminoethoxy-phenyl]-1,2-diphenyl-1-butene), an anti-oestrogen compound (IC50=0.57 microM). 5. Gd3+ antagonized VSOR Cl- current more potently than La3+. The IC50 for Gd3+ was 23 microM. In contrast, 100 microM La3+ inhibited current only 35+/-7%. 6. Antagonists of VSOR Cl- current had non-specific effects. These compounds blocked voltage-dependent K+ and Ca2+ currents in colonic myocytes. Tamoxifen (10 microM) and DIDS (10 microM) inhibited L-type Ca2+ current 87+/-7 and 31+/-5%, respectively. Additionally, in the presence of 300 nM charybdotoxin, tamoxifen (1 microM) and DIDS (10 microM) inhibited delayed rectifier K+ current 38+/-8 and 10+/-2%, respectively. 7. The pharmacology of VSOR Cl- channels overlaps with voltage-dependent cation channels. DIDS and tamoxifen inhibited VSOR Cl- equally. However, because DIDS had much less effect on L-type Ca2+ and delayed rectifier K+ channels than did tamoxifen, it might be useful in experiments to investigate the physiological and pathophysiological role of this conductance in whole tissues.

Indexed as

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAnimalsAntiportersCalcium Channel BlockersCalcium ChannelsChloride ChannelsColonDogsFemaleHypotonic SolutionsIsotonic SolutionsMaleMuscle, SmoothPatch-Clamp TechniquesPotassium Channel BlockersPotassium Channels4,4'-Diisothiocyanostilbene-2,2'-Disulfonic AcidAntiportersCalcium Channel BlockersCalcium ChannelsChloride ChannelsHypotonic SolutionsIsotonic SolutionsPotassium Channel BlockersPotassium Channels

Identifiers

PMID10482912
PMCPMC1566175
OpenAlexW2058758240

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.