Evidence map›Paper›PMID 27497848›Full record

ArticlePflugers Archiv : European journal of physiology2016

Functional coupling of TRPV4 channels and BK channels in regulating spontaneous contractions of the guinea pig urinary bladder.

Ayu Isogai, Ken Lee, Retsu Mitsui, Hikaru Hashitani

Abstract read
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In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2016. 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
2.0field-weighted citation impact, top 16% 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, 30 citations in OpenAlex.

  1. Review
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  12. TRPV4 receptor as a functional sensory molecule in bladder urothelium: Stretch-independent, tissue-specific actions and pathological implications.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  13. TRP Channels as Lower Urinary Tract Sensory Targets.Medical sciences (Basel, Switzerland) · 2019
    Review
  14. Article
  15. Article
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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.

Ayu IsogaiDepartment of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Ken LeeDepartment of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Retsu MitsuiDepartment of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan.
Hikaru HashitaniDepartment of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University, Nagoya, 467-8601, Japan. hasitani@med.nagoya-cu.ac.jp.
Nagoya City University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the role of TRPV4 channels (TRPV4) in regulating the contractility of detrusor smooth muscle (DSM) and muscularis mucosae (MM) of the urinary bladder. Distribution of TRPV4 in DSM and MM of guinea-pig bladders was examined by fluorescence immunohistochemistry. Changes in the contractility of DSM and MM bundles were measured using isometric tension recording. Intracellular Ca(2+) dynamics were visualized by Cal-520 fluorescent Ca(2+) imaging, while membrane potential changes were recorded using intracellular microelectrode technique. DSM and MM expressed TRPV4 immunoreactivity. GSK1016790A (GSK, 1 nM), a TRPV4 agonist, evoked a sustained contraction in both DSM and MM associated with a cessation of spontaneous phasic contractions in a manner sensitive to HC-067047 (10 μM), a TRPV4 antagonist. Iberiotoxin (100 nM) and paxilline (1 μM), large conductance Ca(2+)-activated K(+) (BK) channel blockers restored the spontaneous contractions in GSK. The sustained contractions in DSM and MM were reduced by nifedipine (10 μM), a blocker of L-type voltage-dependent Ca(2+) channels (LVDCCs) by about 40 % and by nominally Ca(2+)-free solution by some 90 %. GSK (1 nM) abolished spontaneous Ca(2+) transients, increased basal Ca(2+) levels and also prevented spontaneous action potential discharge associated with DSM membrane hyperpolarization. In conclusion, Ca(2+) influx through TRPV4 appears to activate BK channels to suppress spontaneous contractions and thus a functional coupling of TRPV4 with BK channels may act as a self-limiting mechanism for bladder contractility during its storage phase. Despite the membrane hyperpolarization in GSK, Ca(2+) entry mainly through TRPV4 develops the tonic contraction.

Indexed as

Muscle ContractionAnimalsCalcium Channel BlockersCalcium ChannelsCalcium SignalingGuinea PigsIndolesLarge-Conductance Calcium-Activated Potassium ChannelsMaleMorpholinesNifedipinePeptidesPotassium Channel BlockersPyrrolesTRPV Cation ChannelsUrinary BladderCalcium Channel BlockersCalcium ChannelsHC-067047iberiotoxinIndolesLarge-Conductance Calcium-Activated Potassium ChannelsMorpholinesNifedipinepaxillinePeptidesPotassium Channel BlockersPyrrolesTRPV Cation ChannelsBK channelsDetrusor smooth muscleMuscularis mucosaeSpontaneous contractionsTRPV4 channels

Identifiers

PMID27497848
OpenAlexW2500376007

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.