Evidence map›Paper›PMID 9831717›Full record

ArticleThe Journal of physiology1999

Monovalent cation and L-type Ca2+ channels participate in calcium paradox-like phenomenon in rabbit aortic smooth muscle cells.

S I Zakharov, D A Mongayt, R A Cohen, V M Bolotina

Abstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. The Mg2+ and Mg(2+)-nucleotide-regulated channel-kinase TRPM7.Handbook of experimental pharmacology · 2007
    Review
  5. Article
  6. Review
  7. Article
  8. 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

4 authors.

S I ZakharovVascular Biology Unit, Department of Medicine, Boston University Medical Center, Boston, MA 02118,, USA.
D A Mongayt
R A Cohen
V M Bolotina

Funding

SCOR IN ISCHEMIC HEART DISEASE IN BLACKSP50HL055993 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI LOSCALZO, JOSEPH · 1995 to 2004
$6.9M
NITRIC OXIDE AND ION CHANNELS IN VASCULAR SMOOTH MUSCLER01HL054150 · NHLBI · BOSTON MEDICAL CENTER · PI BOLOTINA, VICTORIA M · 1996 to 2013
$4.8M
NHLBI NIH HHS HL54150-02NHLBI NIH HHS HL55993-02NHLBI NIH HHS P50 HL055993NHLBI NIH HHS R01 HL054150PHS HHS H31607-15
6 · The paper itself

Abstract

1. The effects of removal of extracellular divalent cations (experimental calcium paradox conditions) were studied on the whole-cell current in freshly isolated smooth muscle cells (SMCs), and on contraction in rabbit aortic rings. 2. Aortic rings treated for 30-60 min with extracellular Ca2+- and Mg2+-free solution contracted following readmission of extracellular Ca2+, even in the presence of nifedipine. 3. In isolated SMCs, the removal of extracellular Ca2+ and Mg2+ induced a non-inactivating whole-cell inward current and membrane depolarization. This current was a monovalent cation (MC) current which reversed at around 0 mV and conducted K+ >= Cs+ > Na+ > Li+. Extracellular divalent cations (Ca2+, Mg2+, Ba2+, Mn2+ and Ni2+) inhibited MC current. 4. Using noise analysis of the whole-cell MC current, the single MC channel conductance was estimated to be < 450 fS. 5. MC current was insensitive to nifedipine, TEA, 4-aminopyridine, SK&F 96365 and S-nitroso-N-acetyl-penicillamine (SNAP), but was decreased by amiloride and low pH. 6. When EGTA was present in Ca2+- and Mg2+-free solution, a significant nifedipine-sensitive Na+ current through L-type Ca2+ channels developed in addition to MC current. 7. It is concluded that upon the removal of extracellular Ca2+ and Mg2+ from resting SMCs, an inward MC current develops allowing Na+ influx and causing SMC depolarization which could be the important steps leading to vessel contraction upon Ca2+ readmission. Addition of EGTA to Ca2+- and Mg2+-free solution greatly potentiates Na+ influx and vessel contraction by allowing additional Na+ influx through L-type Ca2+ channels which are activated presumably by MC current-induced depolarization.

Indexed as

4-AminopyridineAnimalsAortaCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCations, MonovalentCesiumChelating AgentsEgtazic AcidGlutamineImidazolesLithiumMagnesiumMembrane Potentials1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid4-AminopyridineCalciumCalcium Channel BlockersCalcium ChannelsCalcium Channels, L-TypeCations, MonovalentCesiumChelating AgentsEgtazic AcidGlutamineImidazolesLithiumMagnesiumNifedipinePenicillaminePotassiumS-nitro-N-acetylpenicillamineSodiumTetraethylammonium

Identifiers

PMID9831717
PMCPMC2269055

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.