Evidence map›Paper›PMID 19761933›Full record

ArticleJournal of the American College of Cardiology2009

The alpha-1D Is the predominant alpha-1-adrenergic receptor subtype in human epicardial coronary arteries.

Brian C Jensen, Philip M Swigart, Marie-Eve Laden, Teresa DeMarco, Charles Hoopes, Paul C Simpson

Open access · greenAbstract read
In one paragraph

Article in Journal of the American College of Cardiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
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  5. Review
  6. Article
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  10. Increased length-dependent activation of human engineered heart tissue after chronic αAmerican journal of physiology. Heart and circulatory physiology · 2023
    Article
  11. Cardiac α1A-adrenergic receptors: emerging protective roles in cardiovascular diseases.American journal of physiology. Heart and circulatory physiology · 2021
    Review
  12. Article
  13. Current Developments on the Role of αFrontiers in cell and developmental biology · 2021
    Review
  14. Article
  15. Review
  16. Article
  17. Pharmacological Properties ofEC pharmacology and toxicology · 2019
    Article
  18. Review
  19. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Brian C JensenSan Francisco VA Medical Center, California 94121, USA.
Philip M Swigart
Marie-Eve Laden
Teresa DeMarco
Charles Hoopes
Paul C Simpson
San Francisco VA Medical Center · USUniversity of California, San Francisco · US

Funding

CATECHOLAMINES AND HYPERTROPHY OF CULTURED HEART CELLSR01HL031113 · NHLBI · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI SIMPSON, PAUL C · 1985 to 2021
$5.7M
Alpha-1-Adrenergic Receptor Subtypes in the Cells of the Human HeartK08HL096836 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI JENSEN, BRIAN C · 2009 to 2013
$663k
NHLBI NIH HHS K08 HL096836NHLBI NIH HHS R01 HL031113
6 · The paper itself

Abstract

objectivesThe goal was to identify alpha-1-adrenergic receptor (AR) subtypes in human coronary arteries.

backgroundThe alpha1-ARs regulate human coronary blood flow. The alpha1-ARs exist as 3 molecular subtypes, alpha1A, alpha1B, and alpha1D, and the alpha1D subtype mediates coronary vasoconstriction in the mouse. However, the alpha1A is thought to be the only subtype in human coronary arteries.

methodsWe obtained human epicardial coronary arteries and left ventricular (LV) myocardium from 19 transplant recipients and 6 unused donors (age 19 to 70 years; 68% male; 32% with coronary artery disease). We cultured coronary rings and human coronary smooth muscle cells. We assayed alpha1- and beta-AR subtype messenger ribonucleic acid (mRNA) by quantitative real-time reverse transcription polymerase chain reaction and subtype proteins by radioligand binding and extracellular signal-regulated kinase (ERK) activation.

resultsThe alpha1D subtype was 85% of total coronary alpha1-AR mRNA and 75% of total alpha1-AR protein, and alpha1D stimulation activated ERK. In contrast, the alpha1D was low in LV myocardium. Total coronary alpha1-AR levels were one-third of beta-ARs, which were 99% the beta2 subtype.

conclusionsThe alpha1D subtype is predominant and functional in human epicardial coronary arteries, whereas the alpha1A and alpha1B are present at very low levels. This distribution is similar to the mouse, where myocardial alpha1A- and alpha1B-ARs mediate beneficial functional responses and coronary alpha1Ds mediate vasoconstriction. Thus, alpha1D-selective antagonists might mediate coronary vasodilation, without the negative cardiac effects of nonselective alpha1-AR antagonists in current use. Furthermore, it could be possible to selectively activate beneficial myocardial alpha1A- and/or alpha1B-AR signaling without causing coronary vasoconstriction.

Indexed as

AdultAgedCase-Control StudiesCoronary Artery DiseaseCoronary VesselsFemaleHeart VentriclesHumansMaleMiddle AgedMyocardiumMyocytes, Smooth MuscleReceptors, Adrenergic, alpha-1Receptors, Adrenergic, betaRNA, MessengerYoung AdultReceptors, Adrenergic, alpha-1Receptors, Adrenergic, betaRNA, Messenger

Identifiers

PMID19761933
PMCPMC2812029
OpenAlexW2090334734

What OpenQuestion holds

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Registered trials

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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.