Evidence map›Paper›PMID 21914438›Full record

ArticleEuropean journal of pharmacology2011

Large conductance Ca2+ -activated K+ channel activation with NS1619 decreases myogenic and neurogenic contractions of rat detrusor smooth muscle.

Rupal P Soder, Georgi V Petkov

Open access · greenAbstract read
In one paragraph

Article in European journal of pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

29 citing papers in PubMed, 41 citations in OpenAlex.

  1. Potential therapeutic targeting of BKMolecular oncology · 2026
    Review
  2. Article
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  8. The Journal of general physiology · 2019
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Central role of the BK channel in urinary bladder smooth muscle physiology and pathophysiology.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. TRPM4 channel: a new player in urinary bladder smooth muscle function in rats.American journal of physiology. Renal physiology · 2013
    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.

Rupal P SoderPharmaceutical & Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, SC 29208, USA.
Georgi V Petkov
University of South Carolina · US

Funding

BK Channel Function and Regulation in Urinary Bladder Smooth MuscleR01DK084284 · NIDDK · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI PETKOV, GEORGI V · 2009 to 2013
$1.6M
Regulation of Urinary Bladder Smooth Muscle by K+ ChannelsR21DK083687 · NIDDK · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI PETKOV, GEORGI V · 2010 to 2011
$393k
NIDDK NIH HHS DK083687NIDDK NIH HHS DK084284NIDDK NIH HHS R01 DK084284NIDDK NIH HHS R21 DK083687
6 · The paper itself

Abstract

Large conductance voltage- and Ca(2+)-activated K(+) (BK) channels are important in regulating detrusor smooth muscle (DSM) function. Here, we examined systematically how the BK channel pharmacological activation modulates DSM contractility. NS1619, a potent BK channel activator, was utilized as a pharmacological tool to investigate the effect of BK channel activation on rat DSM contractility. Isometric tension recordings of DSM strips isolated from rat urinary bladder were performed systematically under various experimental conditions. NS1619 (30 μM) substantially diminished DSM spontaneous contraction amplitude, muscle force integral, frequency, duration and muscle tone. This effect was blocked by iberiotoxin, a BK channel selective inhibitor. NS1619 inhibited the phasic and tonic contractions in DSM strips pre-contracted with either the cholinergic agonist, carbachol (0.1 μM), or the depolarizing agent, KCl (20mM). In the presence of elevated KCl (60 mM KCl), the inhibitory effect of NS1619 was significantly reduced, indicating that BK channel activation is the underlying mechanism of NS1619 action. BK channel activation with NS1619 dramatically decreased the amplitude of electrical field stimulation (EFS)-induced contractions under a range of stimulation frequencies (0.5-50 Hz). In the presence of specific neurotransmitter inhibitors, BK channel activation with NS1619 significantly decreased both cholinergic and purinergic components of EFS-induced contractions. We conclude that BK channel activation with NS1619 significantly inhibited spontaneous, pharmacologically induced and nerve-evoked DSM contractions. Targeting the BK channel with selective openers may offer a unique opportunity to control DSM contractile activity, including pathophysiological conditions such as overactive bladder and detrusor overactivity, regardless of the underlying cause.

Indexed as

AnimalsBenzimidazolesCarbacholCholineCholinergic AgonistsIn Vitro TechniquesIon Channel GatingLarge-Conductance Calcium-Activated Potassium ChannelsMaleMuscle ContractionMyocytes, Smooth MuscleNervous System Physiological PhenomenaPotassiumPurinesRatsSwineBenzimidazolesCarbacholCholineCholinergic AgonistsLarge-Conductance Calcium-Activated Potassium ChannelsNS 1619PotassiumPurines

Identifiers

PMID21914438
PMCPMC3193563
OpenAlexW1995503637

What OpenQuestion holds

Textmetadata
LicenceTDM
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.