Evidence map›Paper›PMID 23703523›Full record

ArticleAmerican journal of physiology. Cell physiology2013

Activation of muscarinic M3 receptors inhibits large-conductance voltage- and Ca2+-activated K+ channels in rat urinary bladder smooth muscle cells.

Shankar P Parajuli, Georgi V Petkov

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Cell physiology, 2013. 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
3.5field-weighted citation impact, top 8% 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, 17 citations in OpenAlex.

  1. Review
  2. Article
  3. The intracellular CaProceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  4. Review
  5. Article
  6. Big-conductance CaChannels (Austin, Tex.) · 2016
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. 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
  13. Article
  14. Article
  15. Article
  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.

Shankar P ParajuliDepartment of Drug Discovery and Biomedical Sciences, South Carolina College of Pharmacy, University of South Carolina, Columbia, South Carolina 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
NIDDK NIH HHS DK-084284NIDDK NIH HHS R01 DK084284
6 · The paper itself

Abstract

Large conductance voltage- and Ca(2+)-activated K(+) (BK) channels are key regulators of detrusor smooth muscle (DSM) contraction and relaxation during urine voiding and storage. Here, we explored whether BK channels are regulated by muscarinic receptors (M-Rs) in native freshly isolated rat DSM cells under physiological conditions using the perforated whole cell patch-clamp technique and pharmacological inhibitors. M-R activation with carbachol (1 μM) initially evoked large transient outward BK currents, followed by inhibition of the spontaneous transient outward BK currents (STBKCs) in DSM cells. Carbachol (1 μM) also inhibited the amplitude and frequency of spontaneous transient hyperpolarizations (STHs) and depolarized the DSM cell membrane potential. Selective inhibition of the muscarinic M3 receptors (M3-Rs) with 4-diphenylacetoxy-N-methylpiperidine (4-DAMP; 0.1 μM), but not muscarinic M2 receptors with methoctramine (1 μM), blocked the carbachol inhibitory effects on STBKCs. Furthermore, blocking the inositol 1,4,5-triphosphate (IP3) receptors with xestospongin-C (1 μM) inhibited the carbachol-induced large transient outward BK currents without affecting carbachol inhibitory effects on STBKCs. Upon pharmacological inhibition of all known cellular sources of Ca(2+) for BK channel activation, carbachol (1 μM) did not affect the voltage-step-induced steady-state BK currents, suggesting that the muscarinic effects in DSM cells are mediated by mobilization of intracellular Ca(2+). In conclusion, our findings provide strong evidence that activation of M3-Rs leads to inhibition of the STBKCs, STHs, and depolarization of DSM cells. Collectively, the data suggest the existence of functional interactions between BK channels and M3-Rs at a cellular level in DSM.

Indexed as

Amphotericin BAnimalsCarbacholCholinergic AgonistsDiaminesEvoked PotentialsGene Expression RegulationLarge-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsMuscarinic AntagonistsMyocytes, Smooth MusclePatch-Clamp TechniquesPiperidinesRatsRats, Sprague-Dawley4-diphenylacetoxy-1,1-dimethylpiperidiniumAmphotericin BCarbacholCholinergic AgonistsDiaminesLarge-Conductance Calcium-Activated Potassium ChannelsmethoctramineMuscarinic AntagonistsPiperidinesReceptor, Muscarinic M34-DAMPdetrusormethoctraminexestospongin-C

Identifiers

PMID23703523
PMCPMC3725628
OpenAlexW2152312901

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.