Evidence map›Paper›PMID 23586426›Full record

ArticleBritish journal of pharmacology2013

Functional expression of KCNQ (Kv7) channels in guinea pig bladder smooth muscle and their contribution to spontaneous activity.

U A Anderson, C Carson, L Johnston, S Joshi, A M Gurney, K D McCloskey

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. KCommunications medicine · 2026
    Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. The Effectiveness in Activating M-Type KInternational journal of molecular sciences · 2021
    Article
  7. Kv7 Channels and Excitability Disorders.Handbook of experimental pharmacology · 2021
    Article
  8. Review
  9. Review
  10. Detrusor Smooth Muscle KFrontiers in physiology · 2020
    Review
  11. Role of KPflugers Archiv : European journal of physiology · 2019
    Article
  12. The KThe Journal of physiology · 2019
    Article
  13. Article
  14. Review
  15. Article
  16. KThe Journal of pharmacology and experimental therapeutics · 2018
    Article
  17. Article
  18. Article
  19. KNaunyn-Schmiedeberg's archives of pharmacology · 2017
    Article
  20. Selective activation of vascular KBritish journal of pharmacology · 2016
    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

6 authors at 2 institutions in 1 country.

U A AndersonCentre for Cancer Research and Cell Biology, School of Medicine, Dentistry and Biomedical Sciences, Queen's University Belfast, Belfast, UK.
C Carson
L Johnston
S Joshi
A M Gurney
K D McCloskey
Queen's University Belfast · GBUniversity of Manchester · GB

Funding

Wellcome TrustWellcome Trust 074591/Z/04Z
6 · The paper itself

Abstract

background and purposeThe aim of the study was to determine whether KCNQ channels are functionally expressed in bladder smooth muscle cells (SMC) and to investigate their physiological significance in bladder contractility. EXPERIMENTAL APPROACH: KCNQ channels were examined at the genetic, protein, cellular and tissue level in guinea pig bladder smooth muscle using RT-PCR, immunofluorescence, patch-clamp electrophysiology, calcium imaging, detrusor strip myography, and a panel of KCNQ activators and inhibitors. KEY

resultsKCNQ subtypes 1-5 are expressed in bladder detrusor smooth muscle. Detrusor strips typically displayed TTX-insensitive myogenic spontaneous contractions that were increased in amplitude by the KCNQ channel inhibitors XE991, linopirdine or chromanol 293B. Contractility was inhibited by the KCNQ channel activators flupirtine or meclofenamic acid (MFA). The frequency of Ca²⁺-oscillations in SMC contained within bladder tissue sheets was increased by XE991. Outward currents in dispersed bladder SMC, recorded under conditions where BK and KATP currents were minimal, were significantly reduced by XE991, linopirdine, or chromanol, and enhanced by flupirtine or MFA. XE991 depolarized the cell membrane and could evoke transient depolarizations in quiescent cells. Flupirtine (20 μM) hyperpolarized the cell membrane with a simultaneous cessation of any spontaneous electrical activity. CONCLUSIONS AND IMPLICATIONS: These novel findings reveal the role of KCNQ currents in the regulation of the resting membrane potential of detrusor SMC and their important physiological function in the control of spontaneous contractility in the guinea pig bladder.

Indexed as

Gene ExpressionMuscle ContractionAnimalsAnimals, Inbred StrainsCalcium SignalingCells, CulturedElectrophysiological PhenomenaGuinea PigsImmunohistochemistryIn Vitro TechniquesKCNQ Potassium ChannelsMaleMembrane PotentialsMembrane Transport ModulatorsMuscle, SmoothMyographyKCNQ Potassium ChannelsMembrane Transport ModulatorsPotassium Channel BlockersProtein Isoforms

Identifiers

PMID23586426
PMCPMC3746117
OpenAlexW2106734313

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.