Evidence map›Paper›PMID 23095462›Full record

ArticleJournal of vascular research2013

Role of TRPC1 and TRPC3 channels in contraction and relaxation of mouse thoracic aorta.

M Y Kochukov, A Balasubramanian, R C Noel, S P Marrelli

Open access · bronzeAbstract read
In one paragraph

Article in Journal of vascular research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.8field-weighted citation impact, top 20% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. The Dysfunction of CaInternational journal of molecular sciences · 2023
    Review
  6. Reduction of TRPC1/TRPC3 mediated CaCellular signalling · 2023
    Article
  7. Article
  8. Article
  9. Article
  10. TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020
    Review
  11. Ischemic Heart Disease and Heart Failure: Role of Coronary Ion Channels.International journal of molecular sciences · 2020
    Review
  12. Article
  13. Calcium signals that determine vascular resistance.Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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.

M Y KochukovDepartment of Anesthesiology, Baylor College of Medicine, Houston, TX 77030, USA.
A Balasubramanian
R C Noel
S P Marrelli
Baylor College of Medicine · US

Funding

Mechanisms of Endothelial Cell HyperpolarizationR01HL088435 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI MARRELLI, SEAN P · 2008 to 2012
$1.9M
NHLBI NIH HHS R01 HL088435
6 · The paper itself

Abstract

BACKGROUND/

aimsCanonical transient receptor potential (TRPC) channels modulate membrane potential and intracellular Ca(2+). We examined the role of TRPC1 and TRPC3 channels in vasocontraction and relaxation in mouse aorta.

methodsVasocontraction and relaxation of aorta from wild-type (WT), TRPC1 KO and TRPC3 knockout (KO) mice were measured for phenylephrine (Phe) and carbachol (CCh). Intracellular Ca(2+) was measured in primary aorta endothelial cells (EC) and whole cell K(+) current in freshly isolated smooth muscle cells (SMC). RESULTS AND

conclusionTRPC1 KO aorta showed increased vasocontraction to Phe compared to WT and TRPC3 KO aorta due to diminished role of BK(Ca) channels. BK(Ca) mRNA (aorta) and whole cell current (SMC) were reduced versus WT. Contraction in WT aorta was increased to TRPC1 KO level by BK(Ca) channel inhibition. Relaxation to CCh was reduced in TRPC1 KO and TRPC3 KO aortas with concomitant reduction in EC Ca(2+) response. Pyr3 (TRPC3 blocker) reduced the Ca(2+) response to CCh in EC from WT, but not TRPC3 KO mice. In summary, TRPC1 attenuates receptor-mediated contraction through activation and/or expression of SMC BK(Ca) channels while TRPC3 does not contribute to receptor-mediated constriction. Both TRPC1 and TRPC3 participate in EC Ca(2+) influx and vasorelaxation of aorta.

Indexed as

VasoconstrictionVasodilationAnimalsAorta, ThoracicCalciumCells, CulturedEndothelial CellsLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsMembrane PotentialsMiceMice, KnockoutMyocytes, Smooth MusclePotassiumPotassium Channel BlockersTRPC Cation ChannelsVasoconstrictor AgentsBKCa protein, mouseCalciumLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsPotassiumPotassium Channel Blockerstransient receptor potential cation channel, subfamily C, member 1TRPC3 cation channelTRPC Cation ChannelsVasoconstrictor AgentsVasodilator Agents

Identifiers

PMID23095462
PMCPMC3556789
OpenAlexW1970957108

What OpenQuestion holds

Textmetadata
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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.