Evidence map›Paper›PMID 21349579›Full record

ArticleCell calcium2011

Regulation of cardiac Ca(2+) channel by extracellular Na(+).

Shahrzad Movafagh, Lars Cleemann, Martin Morad

Abstract read
In one paragraph

Article in Cell calcium, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Hyponatremia in the Dialysis Population.Kidney international reports · 2019
    Review
  11. Article
  12. Serum sodium and mortality in a national peritoneal dialysis cohort.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2017
    Observational
  13. Pre-dialysis serum sodium and mortality in a national incident hemodialysis cohort.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2016
    Observational
  14. Article
  15. Hyponatremia, mineral metabolism, and mortality in incident maintenance hemodialysis patients: a cohort study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2013
    Article
  16. Outcomes of correcting hyponatremia in patients with myocardial infarction.Clinical research in cardiology : official journal of the German Cardiac Society · 2013
    Article
  17. 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 3 institutions in 1 country.

Shahrzad MovafaghDepartment of Pharmacology, Georgetown University Medical Center, Washington, DC 20007, USA.
Lars Cleemann
Martin Morad
Clemson University · USGeorgetown University · USMedical University of South Carolina · US

Funding

ELECTROPHYSIOLOGY OF NEONATAL AND ADULT HEARTSR01HL016152 · NHLBI · UNIVERSITY OF SOUTH CAROLINA AT COLUMBIA · PI MORAD, MARTIN · 1985 to 2014
$4.5M
Differential 02 Sensing in Right and Left hearts: Crosstalk with Ca-SignalingF32HL088855 · NHLBI · GEORGETOWN UNIVERSITY · PI MOVAFAGH, SHAHRZAD · 2007 to 2009
$174k
NHLBI NIH HHS 5 F32HL088855NHLBI NIH HHS F32 HL088855NHLBI NIH HHS HL-16152NHLBI NIH HHS R01 HL016152
6 · The paper itself

Abstract

Hyponatremia is a predictor of poor cardiovascular outcomes during acute myocardial infarction and in the setting of preexisting heart failure [1]. There are no definitive mechanisms as to how hyponatremia suppresses cardiac function. In this report we provide evidence for direct down-regulation of Ca(2+) channel current in response to low serum Na(+). In voltage-clamped rat ventricular myocytes or HEK 293 cells expressing the L-type Ca(2+) channel, a 15mM drop in extracellular Na(+) suppressed the Ca(2+) current by ∼15%; with maximal suppression of ∼30% when Na(+) levels were reduced to 100mM or less. The suppressive effects of low Na(+) on I(Ca), in part, depended on the substituting monovalent species (Li(+), Cs(+), TEA(+)), but were independent of phosphorylation state of the channel and possible influx of Ca(2+) on Na(+)/Ca(2+) exchanger. Acidification sensitized the Ca(2+) channel current to Na(+) withdrawal. Collectively our data suggest that Na(+) and H(+) may interact with regulatory site(s) at the outer recesses of the Ca(2+) channel pore thereby directly modulating the electro-diffusion of the permeating divalents (Ca(2+), Ba(2+)).

Indexed as

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterAnimalsCalciumCalcium Channel AgonistsCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesElectrophysiological PhenomenaHEK293 CellsHumansMaleMyocytes, CardiacPhosphorylationRatsRats, WistarRecombinant ProteinsSodium3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl esterCalciumCalcium Channel AgonistsCalcium Channels, L-TypeCyclic AMP-Dependent Protein KinasesRecombinant ProteinsSodiumSodium-Calcium Exchanger

Identifiers

PMID21349579
PMCPMC3062524
OpenAlexW1989956720

What OpenQuestion holds

Textmetadata
LicenceTDM
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.