Evidence map›Paper›PMID 8894977›Full record

ArticleThe Journal of general physiology1996

Redox modulation of L-type calcium channels in ferret ventricular myocytes. Dual mechanism regulation by nitric oxide and S-nitrosothiols.

D L Campbell, J S Stamler, H C Strauss

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 125 papers.

0numbers the graph read from it
0cells of the map it votes in
125citing papers in PubMed
11.6field-weighted citation impact, top 1% 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

125 citing papers in PubMed, 442 citations in OpenAlex.

  1. Mechanotransduction-Driven Modulation ofInternational journal of molecular sciences · 2025
    Article
  2. Modulation of Redox-Sensitive Cardiac Ion Channels.Antioxidants (Basel, Switzerland) · 2025
    Review
  3. Redox Regulation of KAntioxidants & redox signaling · 2024
    Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Regulation of Ion Channel Function by Gas Molecules.Advances in experimental medicine and biology · 2021
    Review
  11. Oxidative Stress Orchestrates MAPK and Nitric-Oxide Synthase Signal.International journal of molecular sciences · 2020
    Review
  12. Review
  13. Review
  14. Role of Oxidative Stress in the Genesis of Ventricular Arrhythmias.International journal of molecular sciences · 2020
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

65 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

3 authors at 1 institution in 1 country.

D L CampbellDepartment of Pharmacology, Duke University Medical Center, Durham, North Carolina 27710, USA.
J S Stamler
H C Strauss
Duke Medical Center · US

Funding

CHARACTERIZATION OF CARDIAC PACEMAKER ACTIVITYR01HL019216 · NHLBI · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI STRAUSS, HAROLD C · 1985 to 2000
$385k
EDRF, NITROSTHIOLS, AND PLATELET FUNCTIONK08HL002582 · NHLBI · DUKE UNIVERSITY · PI STAMLER, JONATHAN S. · 1991 to 1995
–
SIGNAL TRANSDUCTION IN VASCULAR SMOOTH MUSCLEP50HL054314 · NHLBI · DUKE UNIVERSITY · PI STRAUSS, HAROLD C · 1995 to 1999
–
CHARACTERIZATION OF CARDIAC PACEMAKER ACTIVITYR37HL019216 · NHLBI · DUKE UNIVERSITY · PI STRAUSS, HAROLD C · 1986 to 1995
–
NHLBI NIH HHS HL02582NHLBI NIH HHS HL19216NHLBI NIH HHS HL54314
6 · The paper itself

Abstract

The effects of NO-related activity and cellular thiol redox state on basal L-type calcium current, ICa,L, in ferret right ventricular myocytes were studied using the patch clamp technique. SIN-1, which generates both NO. and O2-, either inhibited or stimulated ICa,L. In the presence of superoxide dismutase only inhibition was seen. 8-Br-cGMP also inhibited ICa,L, suggesting that the NO inhibition is cGMP-dependent. On the other hand, S-nitrosothiols (RSNOs), which donate NO+, stimulated ICa,L. RSNO effects were not dependent upon cell permeability, modulation of SR Ca2+ release, activation of kinases, inhibition of phosphatases, or alterations in cGMP levels. Similar activation of ICa,L by thiol oxidants, and reversal by thiol reductants, identifies an allosteric thiol-containing "redox switch" on the L-type calcium channel subunit complex by which NO/O2- and NO+ transfer can exert effects opposite to those produced by NO. In sum, our results suggest that: (a) both indirect (cGMP-dependent) and direct (S-nitrosylation/oxidation) regulation of ventricular ICa,L, and (b) sarcolemma thiol redox state may be an important determinant of ICa,L activity.

Indexed as

AnimalsCalcium ChannelsExtracellular SpaceFerretsHeart VentriclesMaleMolsidomineMyocardiumNitric OxideNitroso CompoundsOxidation-ReductionPatch-Clamp TechniquesSulfhydryl CompoundsCalcium ChannelslinsidomineMolsidomineNitric OxideNitroso CompoundsSulfhydryl Compounds

Identifiers

PMID8894977
PMCPMC2229328
OpenAlexW2143855170

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.