Evidence map›Paper›PMID 25080489›Full record

ArticleAmerican journal of physiology. Cell physiology2014

Angiotensin II modulates mouse skeletal muscle resting conductance to chloride and potassium ions and calcium homeostasis via the AT1 receptor and NADPH oxidase.

Anna Cozzoli, Antonella Liantonio, Elena Conte, Maria Cannone, Ada Maria Massari, Arcangela Giustino, Antonia Scaramuzzi, Sabata Pierno, Paola Mantuano, Roberta Francesca Capogrosso and 2 more

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Pharmacotherapy of the Lipid-Lowering Drugs: Update on Efficacy and Risk.International journal of molecular sciences · 2023
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Skeletal muscle ClC-1 chloride channels in health and diseases.Pflugers Archiv : European journal of physiology · 2020
    Review
  10. Article
  11. Review
  12. Muscle wasting: A review of exercise, classical and non-classical RAS axes.Journal of cellular and molecular medicine · 2019
    Review
  13. Acute ATJournal of molecular and cellular cardiology · 2019
    Article
  14. The Renin-Angiotensin System and Skeletal Muscle.Exercise and sport sciences reviews · 2018
    Review
  15. Article
  16. Review
  17. Intracellular calcium increases in vascular smooth muscle cells with progression of chronic kidney disease in a rat model.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Article
  18. Article
  19. Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016
    Review
  20. 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

12 authors at 1 institution in 1 country.

Anna CozzoliUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Antonella LiantonioUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Elena ConteUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Maria CannoneUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Ada Maria MassariUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Arcangela GiustinoDepartment of Biomedical Sciences and Human Oncology, University of Bari "A. Moro," Bari, Italy.
Antonia ScaramuzziUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Sabata PiernoUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Paola MantuanoUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Roberta Francesca CapogrossoUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Giulia Maria CamerinoUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and.
Annamaria De LucaUnit of Pharmacology, Department of Pharmacy and Drug Sciences, University of Bari "A. Moro," Bari, Italy; and annamaria.deluca@uniba.it.
University of Bari Aldo Moro · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiotensin II (ANG II) plays a role in muscle wasting and remodeling; however, little evidence shows its direct effects on specific muscle functions. We presently investigated the acute in vitro effects of ANG II on resting ionic conductance and calcium homeostasis of mouse extensor digitorum longus (EDL) muscle fibers, based on previous findings that in vivo inhibition of ANG II counteracts the impairment of macroscopic ClC-1 chloride channel conductance (gCl) in the mdx mouse model of muscular dystrophy. By means of intracellular microelectrode recordings we found that ANG II reduced gCl in the nanomolar range and in a concentration-dependent manner (EC50 = 0.06 μM) meanwhile increasing potassium conductance (gK). Both effects were inhibited by the ANG II receptors type 1 (AT1)-receptor antagonist losartan and the protein kinase C inhibitor chelerythrine; no antagonism was observed with the AT2 antagonist PD123,319. The scavenger of reactive oxygen species (ROS) N-acetyl cysteine and the NADPH-oxidase (NOX) inhibitor apocynin also antagonized ANG II effects on resting ionic conductances; the ANG II-dependent gK increase was blocked by iberiotoxin, an inhibitor of calcium-activated potassium channels. ANG II also lowered the threshold for myofiber and muscle contraction. Both ANG II and the AT1 agonist L162,313 increased the intracellular calcium transients, measured by fura-2, with a two-step pattern. These latter effects were not observed in the presence of losartan and of the phospholipase C inhibitor U73122 and the in absence of extracellular calcium, disclosing a Gq-mediated calcium entry mechanism. The data show for the first time that the AT1-mediated ANG II pathway, also involving NOX and ROS, directly modulates ion channels and calcium homeostasis in adult myofibers.

Indexed as

Angiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsCalciumCalcium SignalingChloridesDose-Response Relationship, DrugEnzyme InhibitorsExcitation Contraction CouplingFree Radical ScavengersHomeostasisMaleMembrane PotentialsMice, Inbred C57BLMuscle Fibers, SkeletalNADPH OxidasesAngiotensin IIAngiotensin II Type 1 Receptor BlockersCalciumChloridesEnzyme InhibitorsFree Radical ScavengersNADPH OxidasesPotassiumReactive Oxygen SpeciesReceptor, Angiotensin, Type 1angiotensin IIAT1 receptorchloride channel conductanceNADPH oxidaseprotein kinase C

Identifiers

PMID25080489
PMCPMC4187056
OpenAlexW2091184840

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.