Evidence map›Paper›PMID 11389195›Full record

ArticleThe Journal of physiology2001

Cyclic GMP regulation of the L-type Ca(2+) channel current in human atrial myocytes.

G Vandecasteele, I Verde, C Rücker-Martin, P Donzeau-Gouge, R Fischmeister

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
3.0field-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

54 citing papers in PubMed, 151 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. New Therapeutics for Heart Failure: Focusing on cGMP Signaling.International journal of molecular sciences · 2023
    Review
  7. Function and Role of Histamine HPharmaceuticals (Basel, Switzerland) · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Imaging of PDE2- and PDE3-Mediated cGMP-to-cAMP Cross-Talk in Cardiomyocytes.Journal of cardiovascular development and disease · 2018
    Review
  19. Article
  20. Reduced density and altered regulation of rat atrial L-type CaAmerican journal of physiology. Heart and circulatory physiology · 2017
    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 4 institutions in 1 country.

G VandecasteeleLaboratoire de Cardiologie Cellulaire et Moléculaire, INSERM U-446, Université de Paris-Sud, Faculté de Pharmacie, F-92296 Châtenay-Malabry, France.
I Verde
C Rücker-Martin
P Donzeau-Gouge
R Fischmeister
Université Paris Cité · FRHôpital Privé Jacques Cartier · FRInserm · FRLaboratoire d'Énergétique Moléculaire et Macroscopique, Combustion · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The regulation of the L-type Ca(2+) current (I(Ca)) by intracellular cGMP was investigated in human atrial myocytes using the whole-cell patch-clamp technique. 2. Intracellular application of 0.5 microM cGMP produced a strong stimulation of basal I(Ca) (+64 +/- 5 %, n = 60), whereas a 10-fold higher cGMP concentration induced a 2-fold smaller increase (+36 +/- 8 %, n = 35). 3. The biphasic response of I(Ca) to cGMP was not mimicked by the cGMP-dependent protein kinase (PKG) activator 8-bromoguanosine 3',5' cyclic monophosphate (8-bromo-cGMP, 0.5 or 5 microM), and was not affected by the PKG inhibitor KT 5823 (100 nM). 4. In contrast, cGMP stimulation of I(Ca) was abolished by intracellular perfusion with PKI (10 microM), a selective inhibitor of the cAMP-dependent protein kinase (PKA). 5. Selective inhibition of the cGMP-inhibited phosphodiesterase (PDE3) by extracellular cilostamide (100 nM) strongly enhanced basal I(Ca) in control conditions (+78 +/- 13 %, n = 7) but had only a marginal effect in the presence of intracellular cGMP (+22 +/- 7 % in addition to 0.5 microM cGMP, n = 11; +20 +/- 22 % in addition to 5 microM cGMP, n = 7). 6. Application of erythro-9-[2-hydroxy-3-nonyl]adenine (EHNA, 30 microM), a selective inhibitor of the cGMP-stimulated phosphodiesterase (PDE2), fully reversed the secondary inhibitory effect of 5 microM cGMP on I(Ca) (+99 +/- 16 % stimulation, n = 7). 7. Altogether, these data indicate that intracellular cGMP regulates basal I(Ca) in human atrial myocytes in a similar manner to NO donors. The effect of cGMP involves modulation of the cAMP level and PKA activity via opposite actions of the nucleotide on PDE2 and PDE3.

Indexed as

3',5'-Cyclic-AMP PhosphodiesterasesAdolescentAdultAgedAged, 80 and overCalcium Channels, L-TypeChildCyclic AMP-Dependent Protein KinasesCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 2Cyclic Nucleotide Phosphodiesterases, Type 3Heart AtriaHumansMiddle AgedMuscle Fibers, Skeletal3',5'-Cyclic-AMP Phosphodiesterases8-bromocyclic GMPCalcium Channels, L-TypecilostamideCyclic AMP-Dependent Protein KinasesCyclic GMPCyclic GMP-Dependent Protein KinasesCyclic Nucleotide Phosphodiesterases, Type 2Cyclic Nucleotide Phosphodiesterases, Type 3PDE2A protein, humanPhosphodiesterase InhibitorsPhosphoric Diester HydrolasesQuinolones

Identifiers

PMID11389195
PMCPMC2278627
OpenAlexW2121763258

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.