Evidence map›Paper›PMID 17496023›Full record

ArticleBiophysical journal2007

Nav channel mechanosensitivity: activation and inactivation accelerate reversibly with stretch.

Catherine E Morris, Peter F Juranka

Abstract read
In one paragraph

Article in Biophysical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing 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

88 citing papers in PubMed.

  1. Spontaneous spiking in photoreceptors of Periplaneta americana.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Intravascular laser lithotripsy for calcium fracture in human coronary arteries.EuroIntervention : journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology · 2023
    Article
  9. Article
  10. Article
  11. PI(4,5)P2 regulates the gating of NaV1.4 channels.The Journal of general physiology · 2023
    Article
  12. Article
  13. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  14. Review
  15. Article
  16. Article
  17. Capsaicin as an amphipathic modulator of NaChannels (Austin, Tex.) · 2022
    Article
  18. Article
  19. Article
  20. Review

28 more citing papers are in PubMed but not listed here.

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.

Catherine E MorrisNeuroscience, Ottawa Health Research Institute, Ottawa, Ontario, Canada. cmorris@ohri.ca
Peter F Juranka

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Voltage-gated sodium channels (Nav) are modulated by many bilayer mechanical amphiphiles, but whether, like other voltage-gated channels (Kv, HCN, Cav), they respond to physical bilayer deformations is unknown. We expressed human heart Nav1.5 pore alpha-subunit in oocytes (where, unlike alphaNav1.4, alphaNav1.5 exhibits normal kinetics) and measured small macroscopic currents in cell-attached patches. Pipette pressure was used to reversibly stretch the membrane for comparison of I(Na)(t) before, during, and after stretch. At all voltages, and in a dose-dependent fashion, stretch accelerated the I(Na)(t) time course. The sign of membrane curvature was not relevant. Typical stretch stimuli reversibly accelerated both activation and inactivation by approximately 1.4-fold; normalization of peak I(Na)(t) followed by temporal scaling ( approximately 1.30- to 1.85-fold) resulted in full overlap of the stretch/no-stretch traces. Evidently the rate-limiting outward voltage sensor motion in the Nav1.5 activation path (as in Kv1) accelerated with stretch. Stretch-accelerated inactivation occurred even with activation saturated, so an independently stretch-modulated inactivation transition is also a possibility. Since Nav1.5 channel-stretch modulation was both reliable and reversible, and required stretch stimuli no more intense than what typically activates putative mechanotransducer channels (e.g., stretch-activated TRPC1-based currents), Nav channels join the ranks of putative mechanotransducers. It is noteworthy that at voltages near the activation threshold, moderate stretch increased the peak I(Na) amplitude approximately 1.5-fold. It will be important to determine whether stretch-modulated Nav current contributes to cardiac arrhythmias, to mechanosensory responses in interstitial cells of Cajal, to touch receptor responses, and to neuropathic (i.e., hypermechanosensitive) and/or normal pain reception.

Indexed as

AnimalsCell MembraneElectrophysiologyFemaleHumansKineticsMuscle ProteinsNAV1.5 Voltage-Gated Sodium ChannelOocytesPatch-Clamp TechniquesRecombinant ProteinsSodium ChannelsTransfectionXenopus laevisMuscle ProteinsNAV1.5 Voltage-Gated Sodium ChannelRecombinant ProteinsSCN5A protein, humanSodium Channels

Identifiers

PMID17496023
PMCPMC1913161

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.