Evidence map›Paper›PMID 9032685›Full record

ArticleThe Journal of physiology1997

Myogenic contraction by modulation of voltage-dependent calcium currents in isolated rat cerebral arteries.

J G McCarron, C A Crichton, P D Langton, A MacKenzie, G L Smith

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1997. 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
3.2field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Article
  3. Increased CaBiochemical pharmacology · 2023
    Article
  4. Review
  5. Article
  6. Endocannabinoids in cerebrovascular regulation.American journal of physiology. Heart and circulatory physiology · 2016
    Review
  7. Review
  8. Reduced vascular smooth muscle BK channel current underlies heart failure-induced vasoconstriction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Cholinergic receptor and cyclic stretch-mediated inflammatory gene expression in intact ASM.American journal of respiratory cell and molecular biology · 2006
    Article
  15. Article
  16. Article
  17. Article
  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

5 authors at 1 institution in 1 country.

J G McCarronDivision of Neuroscience and Biomedical Systems, University of Glasgow, UK. J.McCarron@biomed.gla.ac.uk
C A Crichton
P D Langton
A MacKenzie
G L Smith
University of Glasgow · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

1. Tissue blood flow and blood pressure are regulated by the spontaneous, myogenic, contraction developed by resistance arteries. However, the cellular mechanisms underlying myogenic contraction are not understood. In this study, the mechanisms of myogenic contraction in cerebral resistance arteries were investigated. 2. The vasoconstriction observed in response to increased pressure in cerebral resistance arteries (myogenic reactivity) was dependent on Ca2+ entry through voltage-dependent Ca2+ channels, since it was abolished by Ca2+ removal and by dihydropyridine antagonists of voltage-dependent Ca2+ channels. 3. Myogenic reactivity persisted in a high-K+ saline, with reduced Ca2+, where membrane potential is presumed to be clamped. Therefore, membrane depolarization alone does not fully account for the increased voltage-dependent Ca2+ channel opening. 4. Voltage-dependent Ca2+ currents in single smooth muscle cells isolated from the resistance artery were substantially increased by applying positive pressure to the patch electrode evoking membrane stretch. 5. Myogenic reactivity remained unaffected by ryanodine and therefore was independent of internal ryanodine-sensitive Ca2+ stores. 6. The myofilament Ca2+ sensitivity was not increased by elevated pressure in alpha-toxin-permeabilized arteries. However, pharmacological activation of protein kinase C or G proteins did increase the myofilament Ca2+ sensitivity. 7. Myogenic contraction over the pressure range 30-70 mmHg could be accounted for by an increase in [Ca2+]i from 100 to 200 nM. 8. It is concluded that modest increases in [Ca2+]i within the range 100-200 nM can account for that myogenic contraction, and that stretch-evoked modulation of Ca2+ currents may contribute to the myogenic response.

Indexed as

Actin CytoskeletonAnimalsCalcium ChannelsCapillary PermeabilityCerebral ArteriesChelating AgentsEgtazic AcidElectrophysiologyIn Vitro TechniquesMaleMembrane PotentialsMuscle ContractionMuscle, Smooth, VascularProtein Kinase CRatsRats, Inbred WKYCalcium ChannelsChelating AgentsEgtazic AcidProtein Kinase CType C Phospholipases

Identifiers

PMID9032685
PMCPMC1159207
OpenAlexW2082837532

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.