Evidence map›Paper›PMID 15293051›Full record

ArticlePflugers Archiv : European journal of physiology2004

Cell-volume-dependent vascular smooth muscle contraction: role of Na+, K+, 2Cl- cotransport, intracellular Cl- and L-type Ca2+ channels.

Yana J Anfinogenova, Mikhail B Baskakov, Igor V Kovalev, Alexander A Kilin, Nickolai O Dulin, Sergei N Orlov

Abstract read
PubMed Publisher
In one paragraph

Article in Pflugers Archiv : European journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
  2. Increased intracellular ClAmerican journal of physiology. Cell physiology · 2021
    Article
  3. Review
  4. Vasoconstriction triggered by hydrogen sulfide: Evidence for NaBiochemistry and biophysics reports · 2017
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Article
  11. SPAK-knockout mice manifest Gitelman syndrome and impaired vasoconstriction.Journal of the American Society of Nephrology : JASN · 2010
    Article
  12. Article
  13. Article
  14. Effect of the Na-K-2Cl cotransporter NKCC1 on systemic blood pressure and smooth muscle tone.American journal of physiology. Heart and circulatory physiology · 2007
    Article
  15. Intracellular monovalent ions as second messengers.The Journal of membrane biology · 2006
    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

6 authors at 3 institutions in 4 countries.

Yana J AnfinogenovaDepartment of Biophysics and Functional Diagnostics, Siberian State Medical University, Tomsk, Russia.
Mikhail B Baskakov
Igor V Kovalev
Alexander A Kilin
Nickolai O Dulin
Sergei N Orlov
Siberian State Medical University · RUUniversité de Montréal · CAUniversity of Chicago · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study elucidates the role of cell volume in contractions of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat aorta. We observed that hyposmotic swelling as well as hyper- and isosmotic shrinkage led to VSMR contractions. Swelling-induced contractions were accompanied by activation of Ca2+ influx and were abolished by nifedipine and verapamil. In contrast, contractions of shrunken cells were insensitive to the presence of L-type channel inhibitors and occurred in the absence of Ca2+ o. Thirty minutes preincubation with bumetanide, a potent Na+, K+, CI- cotransport (NKCC) inhibitor, decreased Cl(-)i content, nifedipine-sensitive 45Ca uptake and contractions triggered by modest depolarization ([K+]o = 36 mM). Elevation of [K+]o to 66 mM completely abolished the effect of bumetanide on these parameters. Bumetanide almost completely abrogated phenylephrine-induced contraction, partially suppressed contractions triggered by hyperosmotic shrinkage, but potentiated contractions of isosmotically shrunken VSMR. Our results suggest that bumetanide suppresses contraction of modestly depolarized cells via NKCC inhibition and Cl(-)i-mediated membrane hyperpolarization, whereas augmented contraction of isosmotically shrunken VSMR by bumetanide is a consequence of suppression of NKCC-mediated regulatory volume increase. The mechanism of bumetanide inhibition of contraction of phenylephrine-treated and hyperosmotically shrunken VSMR should be examined further.

Indexed as

Cell SizeMuscle, Smooth, VascularAnimalsAortaCalcium Channels, L-TypeCells, CulturedChloridesCulture MediaHypertonic SolutionsHypotonic SolutionsIn Vitro TechniquesMuscle ContractionPotassiumProtein IsoformsRatsRats, WistarCalcium Channels, L-TypeChloridesCulture MediaHypertonic SolutionsHypotonic SolutionsPotassiumProtein IsoformsSlc12a2 protein, ratSodiumSodium-Potassium-Chloride SymportersSolute Carrier Family 12, Member 2

Identifiers

PMID15293051
OpenAlexW2042891921

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.