Evidence map›Paper›PMID 28482351›Full record

ReviewJournal of cardiovascular pharmacology2017

Communication Is Key: Mechanisms of Intercellular Signaling in Vasodilation.

Julie K Freed, David D Gutterman

Abstract readReview
In one paragraph

Review in Journal of cardiovascular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Trial
  2. Heavy alcohol consumption attenuates human mesenteric artery responsiveness to sigma receptor-1 ligands.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Intracellular communication and immunothrombosis in sepsis.Journal of thrombosis and haemostasis : JTH · 2022
    Review
  10. Article
  11. Review
  12. Article
  13. Oxidative Stress: A Unifying Paradigm in Hypertension.The Canadian journal of cardiology · 2020
    Review
  14. Review
  15. 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

2 authors.

Julie K FreedDepartments of *Anesthesiology; and†Medicine, Cardiology Division, and Cardiovascular Center, Medical College of Wisconsin, Milwaukee, WI.
David D Gutterman

Funding

Flow-Mediated Dilation of Human Coronary ArteriolesR01HL080704 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2006 to 2010
$1.8M
Novel Regulatory Mechanisms in the Human MicrocirculationR01HL135901 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2017 to 2020
$1.7M
Role of Hydrogen Peroxide in the Mechanism of Flow-Induced Dilation of the Human R01HL094971 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2009 to 2012
$1.5M
High glucose and arteriolar Kv channelsR01HL067968 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GUTTERMAN, DAVID D. · 2003 to 2006
$1.4M
NHLBI NIH HHS L30 HL133387NHLBI NIH HHS R01 HL067968NHLBI NIH HHS R01 HL080704NHLBI NIH HHS R01 HL094971NHLBI NIH HHS R01 HL135901
6 · The paper itself

Abstract

Thirty years ago, Robert F. Furchgott concluded that nitric oxide, a compound traditionally known to be a toxic component of fuel exhaust, is in fact released from the endothelium, and in a paracrine fashion, induces relaxation of underlying vascular smooth muscle resulting in vasodilation. This discovery has helped pave the way for a more thorough understanding of vascular intercellular and intracellular communication that supports the process of regulating regional perfusion to match the local tissue oxygen demand. Vasoregulation is controlled not only by endothelial release of a diverse class of vasoactive compounds such as nitric oxide, arachidonic acid metabolites, and reactive oxygen species, but also by physical forces on the vascular wall and through electrotonic conduction through gap junctions. Although the endothelium is a critical source of vasoactive compounds, paracrine mediators can also be released from surrounding parenchyma such as perivascular fat, myocardium, and cells in the arterial adventitia to exert either local or remote vasomotor effects. The focus of this review will highlight the various means by which intercellular communication contributes to mechanisms of vasodilation. Paracrine signaling and parenchymal influences will be reviewed as well as regional vessel communication through gap junctions, connexons, and myoendothelial feedback. More recent modes of communication such as vesicular and microRNA signaling will also be discussed.

Indexed as

Signal TransductionVasodilationAnimalsArteriesCardiovascular DiseasesEndothelium-Dependent Relaxing FactorsEndothelium, VascularHumansMuscle, Smooth, VascularNitric OxideParacrine CommunicationReactive Oxygen SpeciesEndothelium-Dependent Relaxing FactorsNitric OxideReactive Oxygen Species

Identifiers

PMID28482351
PMCPMC5424612

What OpenQuestion holds

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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.