Evidence map›Paper›PMID 18204472›Full record

ArticleBritish journal of pharmacology2008

Methionine and its derivatives increase bladder excitability by inhibiting stretch-dependent K(+) channels.

S A Baker, G W Hennig, J Han, F C Britton, T K Smith, S D Koh

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Pacemaking in the lymphatic system.The Journal of physiology · 2026
    Review
  2. Article
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  4. Article
  5. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  6. Review
  7. Article
  8. Review
  9. Article
  10. Altered expression and modulation of the two-pore-domain (KAmerican journal of physiology. Renal physiology · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. TREK-1 currents in smooth muscle cells from pregnant human myometrium.American journal of physiology. Cell physiology · 2013
    Article
  17. Article
  18. Review
  19. Review
  20. Colitis decreases mechanosensitive K2P channel expression and function in mouse colon sensory neurons.American journal of physiology. Gastrointestinal and liver physiology · 2011
    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 1 institution in 1 country.

S A BakerDepartment of Physiology and Cell Biology, University of Nevada School of Medicine, Reno, NV 89557, USA.
G W Hennig
J Han
F C Britton
T K Smith
S D Koh
University of Nevada, Reno · US

Funding

STRETCH DEPENDENT POTASSIUM CHANNEL REGULATION IN OVERACTIVE BLADDERP20RR018751 · NCRR · UNIVERSITY OF NEVADA RENO · PI KOH, SANG DON · 2003 to 2011
$17.3M
NCRR NIH HHS P20 RR018751NCRR NIH HHS P20 RR 18751
6 · The paper itself

Abstract

background and purposeDuring the bladder filling phase, the volume of the urinary bladder increases dramatically, with only minimal increases in intravesical pressure. To accomplish this, the smooth muscle of the bladder wall must remain relaxed during bladder filling. However, the mechanisms responsible for the stabilization of bladder excitability during stretch are unclear. We hypothesized that stretch-dependent K(+) (TREK) channels in bladder smooth muscle cells may inhibit contraction in response to stretch. EXPERIMENTAL APPROACHES: Bladder tissues from mouse, guinea pig and monkey were used for molecular, patch clamp, mechanical, electrical, Ca(2+) imaging and cystometric responses to methionine and its derivatives, which are putative blockers of stretch-dependent K(+) (SDK) channels. KEY

resultsSDK channels are functionally expressed in bladder myocytes. The single channel conductance of SDK channels is 89pS in symmetrical K(+) conditions and is blocked by L-methionine. Expressed TREK-1 currents are also inhibited by L-methioninol. All three types of bladder smooth muscle cells from mouse, guinea pig and monkey expressed TREK-1 genes. L-methionine, methioninol and methionine methyl ester but not D-methionine increased contractility in concentration-dependent manner. Methioninol further increased contractility and depolarized the membrane in the presence of blockers of Ca(2+)-activated K(+) conductance. L-methionine induced Ca(2+) waves that spread long distances through the tissue under stretched conditions and were associated with strong contractions. In cystometric assays, methioninol injection increased bladder excitability mimicking overactive bladder activity. CONCLUSIONS AND IMPLICATIONS: Methioninol-sensitive K(+) (SDK, TREK-1) channels appear to be important to prevent spread of excitation through the syncitium during bladder filling.

Indexed as

AnimalsCalciumDose-Response Relationship, DrugFemaleGene ExpressionGuinea PigsMacaca fascicularisMaleMethionineMiceMuscle ContractionMuscle, SmoothPatch-Clamp TechniquesPotassium Channel BlockersPotassium Channels, Tandem Pore DomainSpecies SpecificityCalciumMethioninemethionine methyl estermethioninolPotassium Channel Blockerspotassium channel protein TREK-1Potassium Channels, Tandem Pore Domain

Identifiers

PMID18204472
PMCPMC2275456
OpenAlexW1500060932

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.