Evidence map›Paper›PMID 12231648›Full record

ArticleThe Journal of physiology2002

Comparative capacitative calcium entry mechanisms in canine pulmonary and renal arterial smooth muscle cells.

Sean M Wilson, Helen S Mason, Gregory D Smith, Neil Nicholson, Louise Johnston, Robert Janiak, Joseph R Hume

Abstract readComparative Study
In one paragraph

Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Long-Term Hypoxia Negatively Influences CaFrontiers in physiology · 2021
    Article
  2. Article
  3. Article
  4. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  5. Article
  6. Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Maturation of intracellular calcium homeostasis in sheep pulmonary arterial smooth muscle cells.American journal of physiology. Lung cellular and molecular physiology · 2008
    Article
  12. Store-operated calcium entry in vascular smooth muscle.British journal of pharmacology · 2008
    Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

7 authors.

Sean M WilsonDepartment of Pharmacology, University of Nevada School of Medicine, Reno, NV 89557, USA.
Helen S Mason
Gregory D Smith
Neil Nicholson
Louise Johnston
Robert Janiak
Joseph R Hume

Funding

CA2+ SIGNALING IN ARTERIAL SMOOTH MUSCLE CELLSF32HL010476 · NHLBI · UNIVERSITY OF NEVADA RENO · PI WILSON, SEAN M · 2001 to 2002
$86k
NHLBI NIH HHS F32 HL010476NHLBI NIH HHS HL-10476NHLBI NIH HHS HL-48254
6 · The paper itself

Abstract

Experiments were performed to determine whether capacitative Ca(2+) entry (CCE) can be activated in canine pulmonary and renal arterial smooth muscle cells (ASMCs) and whether activation of CCE parallels the different functional structure of the sarcoplasmic reticulum (SR) in these two cell types. The cytosolic [Ca(2+)] was measured by imaging fura-2-loaded individual cells. Increases in the cytosolic [Ca(2+)] due to store depletion in pulmonary ASMCs required simultaneous depletion of both the inositol 1,4,5-trisphosphate (InsP(3))- and ryanodine (RY)-sensitive SR Ca(2+) stores. In contrast, the cytosolic [Ca(2+)] rises in renal ASMCs occurred when the SR stores were depleted through either the InsP(3) or RY pathways. The increase in the cytosolic [Ca(2+)] due to store depletion in both pulmonary and renal ASMCs was present in cells that were voltage clamped and was abolished when cells were perfused with a Ca(2+)-free bathing solution. Rapid quenching of the fura-2 signal by 100 microM Mn(2+) following SR store depletion indicated that extracellular Ca(2+) entry increased in both cell types and also verified that activation of CCE in pulmonary ASMCs required the simultaneous depletion of the InsP(3)- and RY-sensitive SR Ca(2+) stores, while CCE could be activated in renal ASMCs by the depletion of either of the InsP(3)- or RY-sensitive SR stores. Store depletion Ca(2+) entry in both pulmonary and renal ASMCs was strongly inhibited by Ni(2+) (0.1-10 mM), slightly inhibited by Cd(2+) (200-500 microM), but was not significantly affected by the voltage-gated Ca(2+) channel (VGCC) blocker nisoldipine (10 microM). The non-selective cation channel blocker Gd(3+) (100 microM) inhibited a portion of the Ca(2+) entry in 6 of 18 renal but not pulmonary ASMCs. These results provide evidence that SR Ca(2+) store depletion activates CCE in parallel with the organization of intracellular Ca(2+) stores in canine pulmonary and renal ASMCs.

Indexed as

AnimalsCalciumCytosolDogsElectrophysiologyExtracellular SpaceFemaleMaleMembrane PotentialsMuscle, Smooth, VascularMyocytes, Smooth MusclePulmonary ArteryRenal ArterySarcoplasmic ReticulumCalcium

Identifiers

PMID12231648
PMCPMC2290529

What OpenQuestion holds

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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.