Evidence map›Paper›PMID 9729619›Full record

ArticleThe Journal of physiology1998

cGMP inhibits IP3-induced Ca2+ release in intact rat megakaryocytes via cGMP- and cAMP-dependent protein kinases.

S Tertyshnikova, X Yan, A Fein

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
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  8. Review
  9. Effect of cGMP on pharmacomechanical coupling in the uterine artery of near-term pregnant sheep.The Journal of pharmacology and experimental therapeutics · 2008
    Article
  10. Article
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  13. Regulation of canonical transient receptor potential isoform 3 (TRPC3) channel by protein kinase G.Proceedings of the National Academy of Sciences of the United States of America · 2004
    Article
  14. Article
  15. Article
  16. Role of cyclic nucleotides in mediating the nitric oxide (II) effects on transmitter release and the electrogenesis of motor nerve endings.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
    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

3 authors at 2 institutions in 1 country.

S TertyshnikovaDepartment of Physiology, University of Connecticut Health Center, Farmington, CT, USA.
X Yan
A Fein
UConn Health · USAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Inhibition of inositol 1,4,5-trisphosphate (IP3) receptor-mediated Ca2+ release by cGMP was examined in intact rat megakaryocytes, by using a combination of single cell fluorescence microscopy to monitor intracellular free calcium ([Ca2+]i) and flash photolysis of caged second messengers. 2. Sodium nitroprusside (SNP), a nitric oxide (NO) donor, and the hydrolysis-resistant cGMP analogue 8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate (pCPT-cGMP) inhibited Ca2+ release induced by photolysis of caged IP3. Neither of them affected the rate of Ca2+ removal from the cytoplasm following photolysis of caged Ca2+. 3. Photolysis of the caged NO donor 3-morpholinosydnonimine (SIN-1) during agonist-induced [Ca2+]i oscillations inhibited Ca2+ release without affecting the rate of Ca2+ uptake and/or extrusion. 4. We conclude that the inhibition of IP3-induced Ca2+ release is the principal mechanism of NO-cGMP-dependent inhibition of [Ca2+]i mobilization. 5. IPG, a specific peptide inhibitor of cGMP-dependent protein kinase (cGMP-PK), blocked the inhibitory effect of pCPT-cGMP, indicating that the inhibition of IP3-induced Ca2+ release by pCPT-cGMP is mediated by cGMP-PK. However, the simultaneous application of both IPG and IP20, a specific peptide inhibitor of cAMP-dependent protein kinase (cAMP-PK), was required to block the inhibitory effect of SNP. These data strongly suggest that NO-cGMP-dependent inhibition of [Ca2+]i mobilization is mediated via the activation of both cGMP-PK and cAMP-PK.

Indexed as

AnimalsBone Marrow CellsCalciumCyclic AMP-Dependent Protein KinasesCyclic GMPCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsInositol 1,4,5-TrisphosphateIn Vitro TechniquesKineticsMegakaryocytesModels, BiologicalMolsidomineNitric Oxide DonorsNitroprussidePhotolysis8-((4-chlorophenyl)thio)cyclic-3',5'-GMPCalciumCyclic AMP-Dependent Protein KinasesCyclic GMPCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsInositol 1,4,5-TrisphosphatelinsidomineMolsidomineNitric Oxide DonorsNitroprussideThionucleotides

Identifiers

PMID9729619
PMCPMC2231186
OpenAlexW2054547644

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.