Evidence map›Paper›PMID 14694141›Full record

ArticleThe Journal of physiology2004

Increase in endothelial cell Ca(2+) in response to mouse cremaster muscle contraction.

Tasmia Duza, Ingrid H Sarelius

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Trial
  2. Cracking the Endothelial Calcium (CaInternational journal of molecular sciences · 2023
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Vessel diameter measurement from intravital microscopy.Annals of biomedical engineering · 2009
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Macromolecule permeability of in situ and excised rodent skeletal muscle arterioles and venules.American journal of physiology. Heart and circulatory physiology · 2006
    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.

Tasmia DuzaDepartment Pharmacology and Physiology, University of Rochester Medical Center, Box 711, Rochester, NY 14642, USA.
Ingrid H Sarelius
University of Rochester · US

Funding

LOCAL MECHANISMS OF ARTERIOLAR CONTROL IN EXERCISER01HL056574 · NHLBI · UNIVERSITY OF ROCHESTER · PI SARELIUS, INGRID H · 1997 to 2001
$450k
NHLBI NIH HHS HL56574
6 · The paper itself

Abstract

We addressed the role of endothelial cells (ECs) in metabolic dilatation of skeletal muscle arterioles in anaesthetized mice in situ. Electrical field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz. Diameter was observed using bright field microscopy. In controls, muscle contraction produced a 15.7 +/- 1.5 microm dilatation from a baseline of 17.4 +/- 1.6 microm. Endothelial denudation (-EC) via intraluminal perfusion of air abolished this response (1.6 +/- 1.2 microm in -EC, P < 0.05), identifying endothelium as the primary vascular cell type initiating the dilatation. To investigate the role of EC Ca(2+) in metabolic dilatation, arteriolar ECs were loaded with Fluo-4 AM or BAPTA AM by intraluminal perfusion, after which blood flow was re-established. Ca(2+) activity of individual ECs was monitored as a function of change from baseline fluorescence using confocal microscopy. In ECs, whole cell Ca(2+) increased (>10%, P < 0.05) during muscle contraction, and localized Ca(2+) transients were increased (>20%, P < 0.05) during the first minute after contraction. Chelation of EC Ca(2+) abolished the dilatations in response to muscle contraction (1.1 +/- 0.7 microm, P < 0.05). Inhibition of P(1) purinergic receptors (with xanthine amine congener) did not alter the rate of onset of the dilatation (P > 0.05) but decreased its magnitude immediately post stimulation (7.1 +/- 0.9 microm, P < 0.05) and during recovery. These findings demonstrate obligatory roles for endothelium and EC Ca(2+) during metabolic dilatation in intact arterioles. Furthermore, they suggest that at least two separate pathways mediate the local response, one of which involves stimulation of endothelial P(1) purinergic receptors via endogenous adenosine produced during muscle activity.

Indexed as

AdenosineAnimalsCalciumCalcium SignalingChelating AgentsElectric StimulationEndothelial CellsExtracellular SpaceIn Vitro TechniquesMaleMiceMice, Inbred C57BLMuscle ContractionMuscle, SkeletalNitric OxidePurinergic P1 Receptor AntagonistsAdenosineCalciumChelating AgentsNitric OxidePurinergic P1 Receptor AntagonistsReceptors, Purinergic P1

Identifiers

PMID14694141
PMCPMC1664834
OpenAlexW1583493714

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.