Evidence map›Paper›PMID 22081702›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Testosterone-induced relaxation of coronary arteries: activation of BKCa channels via the cGMP-dependent protein kinase.

Viju Deenadayalu, Yashoda Puttabyatappa, Alexander T Liu, John N Stallone, Richard E White

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 57 citations in OpenAlex.

  1. Review
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  6. Article
  7. Review
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  9. Review
  10. Review
  11. Review
  12. Article
  13. Vascular Pathways of Testosterone: Clinical Implications.Journal of cardiovascular translational research · 2020
    Review
  14. Article
  15. Modulatory influence of sex hormones on vascular aging.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  16. Calcium- and voltage-gated BK channels in vascular smooth muscle.Pflugers Archiv : European journal of physiology · 2018
    Review
  17. Article
  18. Article
  19. Review
  20. Review
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

5 authors at 3 institutions in 1 country.

Viju DeenadayaluDepartment of Physiology & Biophysics, Wright State University School of Medicine, Dayton, Ohio, USA.
Yashoda Puttabyatappa
Alexander T Liu
John N Stallone
Richard E White
Augusta University · USTexas A&M University · USWright State University · US

Funding

NONGENOMIC MECHANISMS OF ANDROGENS IN THE VASCULAR WALLR01HL080402 · NHLBI · TEXAS A&M AGRILIFE RESEARCH · PI STALLONE, JOHN NICHOLAS · 2006 to 2009
$1.4M
NHLBI NIH HHS HL-080402
6 · The paper itself

Abstract

Androgens are reported to have both beneficial and detrimental effects on human cardiovascular health. The aim of this study was to characterize nongenomic signaling mechanisms in coronary artery smooth muscle (CASM) and define the ionic basis of testosterone (TES) action. TES-induced relaxation of endothelium-denuded porcine coronary arteries was nearly abolished by 20 nM iberiotoxin, a highly specific inhibitor of large-conductance, calcium-activated potassium (BK(Ca)) channels. Molecular patch-clamp studies confirmed that nanomolar concentrations of TES stimulated BK(Ca) channel activity by ∼100-fold and that inhibition of nitric oxide synthase (NOS) activity by N(G)-monomethyl-L-arginine nearly abolished this effect. Inhibition of nitric oxide (NO) synthesis or guanylyl cyclase activity also attenuated TES-induced coronary artery relaxation but did not alter relaxation due to 8-bromo-cGMP. Furthermore, we detected TES-stimulated NO production in porcine coronary arteries and in human CASM cells via stimulation of the type 1 neuronal NOS isoform. Inhibition of the cGMP-dependent protein kinase (PKG) attenuated TES-stimulated BK(Ca) channel activity, and direct assay determined that TES increased activity of PKG in a concentration-dependent fashion. Last, the stimulatory effect of TES on BK(Ca) channel activity was mimicked by addition of purified PKG to the cytoplasmic surface of a cell-free membrane patch from CASM myocytes (∼100-fold increase). These findings indicate that TES-induced relaxation of endothelium-denuded coronary arteries is mediated, at least in part, by enhanced NO production, leading to cGMP synthesis and PKG activation, which, in turn, opens BK(Ca) channels. These findings provide a molecular mechanism that could help explain why androgens have been reported to relax coronary arteries and relieve angina pectoris.

Indexed as

VasodilationAnimalsCoronary VesselsCyclic GMP-Dependent Protein KinasesDose-Response Relationship, DrugEnzyme ActivationEnzyme InhibitorsFemaleGuanylate CyclaseLarge-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsMuscle, Smooth, VascularNitric OxideNitric Oxide SynthasePatch-Clamp TechniquesCyclic GMP-Dependent Protein KinasesEnzyme InhibitorsGuanylate CyclaseLarge-Conductance Calcium-Activated Potassium ChannelsNitric OxideNitric Oxide SynthasePotassium ChannelsTestosterone

Identifiers

PMID22081702
PMCPMC3334243
OpenAlexW2068420355

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.