Evidence map›Paper›PMID 18790848›Full record

ArticleBiophysical journal2008

Impaired Ca2+-dependent activation of large-conductance Ca2+-activated K+ channels in the coronary artery smooth muscle cells of Zucker Diabetic Fatty rats.

Tong Lu, Dan Ye, Tongrong He, Xiao-li Wang, Hai-long Wang, Hon-Chi Lee

Open access · bronzeAbstract read
In one paragraph

Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Impact of Sorbs2 dysfunction on cardiovascular diseases.Biochimica et biophysica acta. Molecular basis of disease · 2025
    Review
  3. Review
  4. Article
  5. Inhibition of big-conductance CaPflugers Archiv : European journal of physiology · 2021
    Article
  6. Coronary Large Conductance CaFrontiers in physiology · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Impaired BKScientific reports · 2017
    Article
  11. Article
  12. Article
  13. Big-conductance CaChannels (Austin, Tex.) · 2016
    Review
  14. Article
  15. Article
  16. Article
  17. Perivascular adipose tissue and coronary vascular disease.Arteriosclerosis, thrombosis, and vascular biology · 2014
    Review
  18. Article
  19. Article
  20. Reduced vascular smooth muscle BK channel current underlies heart failure-induced vasoconstriction in mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2013
    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

6 authors at 2 institutions in 1 country.

Tong LuDepartment of Internal Medicine, Mayo Clinic, Rochester, Minnesota 55905, USA. lu.tong@mayo.edu
Dan Ye
Tongrong He
Xiao-li Wang
Hai-long Wang
Hon-Chi Lee
Mayo Clinic · USMayo Clinic in Florida · US

Funding

Type 2 Diabetes and Vascular BK Channel RegulationR01HL074180 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2003 to 2018
$4.8M
Endothelial BK Channel Regulation by Caveolae TargetingR01HL080118 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2006 to 2010
$1.8M
Regulation of Vascular BK Channels in DiabetesR56HL074180 · NHLBI · MAYO CLINIC ROCHESTER · PI LEE, HON-CHI · 2008 to 2008
$378k
NHLBI NIH HHS HL-080118NHLBI NIH HHS HL-74180NHLBI NIH HHS R01 HL074180NHLBI NIH HHS R01 HL080118NHLBI NIH HHS R56 HL074180
6 · The paper itself

Abstract

The large-conductance Ca(2+)-activated K(+) (BK) channels play an important role in the regulation of cellular excitability in response to changes in intracellular metabolic state and Ca(2+) homeostasis. In vascular smooth muscle, BK channels are key determinants of vasoreactivity and vital-organ perfusion. Vascular BK channel functions are impaired in diabetes mellitus, but the mechanisms underlying such changes have not been examined in detail. We examined and compared the activities and kinetics of BK channels in coronary arterial smooth muscle cells from Lean control and Zucker Diabetic Fatty (ZDF) rats, using single-channel recording techniques. We found that BK channels in ZDF rats have impaired Ca(2+) sensitivity, including an increased free Ca(2+) concentration at half-maximal effect on channel activation, a reduced steepness of Ca(2+) dose-dependent curve, altered Ca(2+)-dependent gating properties with decreased maximal open probability, and a shortened mean open-time and prolonged mean closed-time durations. In addition, the BK channel beta-subunit-mediated activation by dehydrosoyasaponin-1 (DHS-1) was lost in cells from ZDF rats. Immunoblotting analysis confirmed a 2.1-fold decrease in BK channel beta(1)-subunit expression in ZDF rats, compared with that of Lean rats. These abnormalities in BK channel gating lead to an increase in the energy barrier for channel activation, and may contribute to the development of vascular dysfunction and complications in type 2 diabetes mellitus.

Indexed as

Ion Channel GatingAnimalsCalciumCoronary VesselsElectric ConductivityGene Expression RegulationHyperglycemiaKineticsLarge-Conductance Calcium-Activated Potassium ChannelsMaleMyocytes, Smooth MuscleRatsRats, ZuckerThermodynamicsCalciumLarge-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID18790848
PMCPMC2586587
OpenAlexW2119209095

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.