Evidence map›Paper›PMID 21300746›Full record

ArticleThe Journal of physiology2011

BK channel β1 subunits regulate airway contraction secondary to M2 muscarinic acetylcholine receptor mediated depolarization.

Iurii Semenov, Bin Wang, Jeremiah T Herlihy, Robert Brenner

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Role of Airway Smooth Muscle in Inflammation Related to Asthma and COPD.Advances in experimental medicine and biology · 2021
    Article
  5. Roles of LRRC26 as an auxiliary γ1-subunit of large-conductance CaAmerican journal of physiology. Lung cellular and molecular physiology · 2020
    Article
  6. Review
  7. Article
  8. Involvement of Allosteric Effect and KInternational journal of molecular sciences · 2018
    Article
  9. Chloroform Extract ofEvidence-based complementary and alternative medicine : eCAM · 2017
    Article
  10. Article
  11. Involvement of CaInternational journal of molecular sciences · 2016
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Treatment of experimental asthma using a single small molecule with anti-inflammatory and BK channel-activating properties.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Iurii SemenovDepartment of Physiology, UT Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA.
Bin Wang
Jeremiah T Herlihy
Robert Brenner
The University of Texas Health Science Center at San Antonio · US

Funding

BK Channel B4 Subunit in the Dentate Gyrus and SeizuresR01NS052574 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI BRENNER, ROBERT · 2007 to 2011
$1.3M
NINDS NIH HHS R01 NS052574NINDS NIH HHS R01NS052574
6 · The paper itself

Abstract

The large conductance calcium- and voltage-activated potassium channel (BK channel) and its smooth muscle-specific β1 subunit regulate excitation–contraction coupling in many types of smooth muscle cells. However, the relative contribution of BK channels to control of M2- or M3-muscarinic acetylcholine receptor mediated airway smooth muscle contraction is poorly understood. Previously, we showed that knockout of the BK channel β1 subunit enhances cholinergic-evoked trachea contractions. Here, we demonstrate that the enhanced contraction of the BK β1 knockout can be ascribed to a defect in BK channel opposition of M2 receptor-mediated contractions. Indeed, the enhanced contraction of β1 knockout is eliminated by specific M2 receptor antagonism. The role of BK β1 to oppose M2 signalling is evidenced by a greater than fourfold increase in the contribution of L-type voltage-dependent calcium channels to contraction that otherwise does not occur with M2 antagonist or with β1 containing BK channels. The mechanism through which BK channels oppose M2-mediated recruitment of calcium channels is through a negative shift in resting voltage that offsets, rather than directly opposes, M2-mediated depolarization. The negative shift in resting voltage is reduced to similar extents by BK β1 knockout or by paxilline block of BK channels. Normalization of β1 knockout baseline voltage with low external potassium eliminated the enhanced M2-receptor mediated contraction. In summary, these findings indicate that an important function of BK/β1 channels is to oppose cholinergic M2 receptor-mediated depolarization and activation of calcium channels by restricting excitation–contraction coupling to more negative voltage ranges.

Indexed as

AnimalsCalcium Channels, L-TypeExcitation Contraction CouplingIndolesIn Vitro TechniquesLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsMembrane PotentialsMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalMuscarinic AntagonistsMuscle ContractionMuscle, SmoothPirenzepinePotassium Channel BlockersCalcium Channels, L-TypeIndolesKcnmb1 protein, mouseLarge-Conductance Calcium-Activated Potassium Channel beta SubunitsMuscarinic AntagonistsotenzepadpaxillinePirenzepinePotassium Channel BlockersReceptor, Muscarinic M2

Identifiers

PMID21300746
PMCPMC3099031
OpenAlexW1575058521

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.