Evidence map›Paper›PMID 16020462›Full record

ArticleThe Journal of physiology2005

Electrophysiological and molecular identification of voltage-gated sodium channels in murine vascular myocytes.

Sohag Saleh, Shuk Yin M Yeung, Sally Prestwich, Vladimír Pucovsky, Iain Greenwood

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

38 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Effects of 4,9-anhydrotetrodotoxin on voltage-gated NaNaunyn-Schmiedeberg's archives of pharmacology · 2018
    Article
  12. Article
  13. Article
  14. Article
  15. Cardiac ion channels.Channels (Austin, Tex.) · 2015
    Review
  16. Article
  17. Article
  18. Article
  19. Maximum shortening velocity of lymphatic muscle approaches that of striated muscle.American journal of physiology. Heart and circulatory physiology · 2013
    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

5 authors at 1 institution in 1 country.

Sohag SalehDivision of Basic Medical Sciences, St George's, University of London, London SW17 0RE, UK.
Shuk Yin M Yeung
Sally Prestwich
Vladimír Pucovsky
Iain Greenwood
St George's, University of London · GB

Funding

Wellcome Trust
6 · The paper itself

Abstract

A voltage-gated Na+ current was characterised in freshly dissociated mouse portal vein (PV) smooth muscle myocytes. The current was found superimposed upon the relatively slow L-type Ca2+ current and was resistant to conventional Ca2+ channel blockers but was abolished by external Na+ replacement and tetrodotoxin (TTX, 1 microM). The molecular identity of the channel responsible for this conductance was determined by RT-PCR where only the transcripts for Na+ channel genes SCN7a, 8a and 9a were detected. The presence of the protein counterparts to the SCN8a and 9a genes (NaV1.6 and NaV1.7, respectively) on the individual smooth muscle myocytes were confirmed in immunocytochemistry, which showed diffuse staining around a predominantly plasmalemmal location. TTX inhibited the action potential in individual myocytes generated in the current clamp mode but isometric tissue tension experiments revealed that TTX (1 and 5 microM) had no effect on the inherent mouse PV rhythmicity. However, the Na+ channel opener veratridine (10 and 50 microM) significantly increased the length of contraction and the interval between contractions. This effect was not influenced by pre-incubation with atropine, prazosin and propranolol, but was reversed by TTX (1 microM) and completely abolished by nicardipine (1 microM). Furthermore, preincubation with the reverse-mode Na+-Ca2+ exchange blocker KB-R7943 (10 microM) also inhibited the veratridine response. We have established for the first time the molecular identity of the voltage-gated Na+ channel in freshly dispersed smooth muscle cells and have shown that these channels can modulate contractility through a novel mechanism of action possibly involving reverse mode Na+-Ca2+ exchange.

Indexed as

Action PotentialsAnimalsCalciumCalcium Channel BlockersDose-Response Relationship, DrugFemaleIon Channel GatingMiceMice, Inbred BALB CMuscle ContractionMuscle, Smooth, VascularMyocytes, Smooth MuscleNAV1.6 Voltage-Gated Sodium ChannelNAV1.7 Voltage-Gated Sodium ChannelNerve Tissue ProteinsNicardipine2-(2-(4-(4-nitrobenzyloxy)phenyl)ethyl)isothiourea methanesulfonateCalciumCalcium Channel BlockersNAV1.6 Voltage-Gated Sodium ChannelNAV1.7 Voltage-Gated Sodium ChannelNerve Tissue ProteinsNicardipineScn8a protein, mouseScn9a protein, mouseSodiumSodium-Calcium ExchangerSodium ChannelsTetrodotoxinThioureaVeratridine

Identifiers

PMID16020462
PMCPMC1474751
OpenAlexW2170771241

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.