Evidence map›Paper›PMID 29453306›Full record

ArticleJournal of the American Heart Association2018

Acute Pressor Response to Psychosocial Stress Is Dependent on Endothelium-Derived Endothelin-1.

Brandon M Fox, Bryan K Becker, Analia S Loria, Kelly A Hyndman, Chunhua Jin, Hannah Clark, Robin Johns, Masashi Yanagisawa, David M Pollock, Jennifer S Pollock

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

18 citing papers in PubMed, 27 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Early life stress blunts time-of-day-specific autonomic function in adult male mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Article
  4. Endothelin receptor antagonism in sickle cell disease: Is the time now?Canadian journal of physiology and pharmacology · 2026
    Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Liver circadian clock disruption alters perivascular adipose tissue gene expression and aortic function in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Article
  14. PTSD as an Endothelial Disease: Insights From COVID-19.Frontiers in cellular neuroscience · 2021
    Review
  15. Endothelin-1 in the pathophysiology of obesity and insulin resistance.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2020
    Review
  16. Article
  17. Elevated plasma endothelin-1 is associated with reduced weight loss post vertical sleeve gastrectomy.Surgery for obesity and related diseases : official journal of the American Society for Bariatric Surgery · 2019
    Article
  18. 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

10 authors at 5 institutions in 2 countries.

Brandon M FoxCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL.
Bryan K BeckerCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL.
Analia S LoriaDepartment of Pharmacology and Nutritional Sciences, University of Kentucky, Lexington, KY.
Kelly A HyndmanCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL.
Chunhua JinCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL.
Hannah ClarkUniversity of Evansville, IN.
Robin JohnsCollege of Nursing, Augusta University, Augusta, GA.
Masashi YanagisawaInternational Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Japan.
David M PollockCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL.
Jennifer S PollockCardio-Renal Physiology and Medicine Section, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, AL jenniferpollock@uabmc.edu.
University of Alabama at Birmingham · USAugusta University · USTsukuba International University · JPUniversity of Evansville · USUniversity of Kentucky · US

Funding

Vascular and renal responses to stressP01HL069999 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI GEORGE, VARGHESE · 2002 to 2018
$31.1M
University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
Research Supplement to Promote DiversityP01HL136267 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2017 to 2021
$11.9M
Renal endothelin receptor-specific function in angiotensin ll-dependent hypertensP01HL095499 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SULLIVAN, JENNIFER C · 2010 to 2014
$11.1M
MECHANISMS OF HYPERTENSION AND CARDIOVASCULAR DISEASEST32HL007457 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Martin E Young · 1985 to 2026
$8.6M
The Role of Endothelin-1 in Sickle Cell DiseaseU01HL117684 · NHLBI · AUGUSTA UNIVERSITY · PI KUTLAR, ABDULLAH, MEILER, STEFFEN · 2013 to 2017
$8.1M
Novel mechanisms of HDAC1 regulation of renal collecting duct functionK01DK105038 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI HYNDMAN, KELLY · 2015 to 2019
$754k
Early Life Stress & Chronic Control of Blood PressureR00HL111354 · NHLBI · UNIVERSITY OF KENTUCKY · PI LORIA, ANALIA · 2013 to 2015
$730k
Novel Mechanisms of Decreased NO Bioavailability in Sickle Cell NephropathyF30DK107194 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI FOX, BRANDON M · 2015 to 2018
$153k
NHLBI NIH HHS P01 HL069999NHLBI NIH HHS P01 HL095499NHLBI NIH HHS P01 HL136267NHLBI NIH HHS R00 HL111354NHLBI NIH HHS T32 HL007457NHLBI NIH HHS U01 HL117684NIDDK NIH HHS F30 DK107194NIDDK NIH HHS K01 DK105038NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

backgroundAcute psychosocial stress provokes increases in circulating endothelin-1 (ET-1) levels in humans and animal models. However, key questions about the physiological function and cellular source of stress-induced ET-1 remain unanswered. We hypothesized that endothelium-derived ET-1 contributes to the acute pressor response to stress via activation of the endothelin A receptor. METHODS AND

resultsAdult male vascular endothelium-specific ET-1 knockout mice and control mice that were homozygous for the floxed allele were exposed to acute psychosocial stress in the form of cage switch stress (CSS), with blood pressure measured by telemetry. An acute pressor response was elicited by CSS in both genotypes; however, this response was significantly blunted in vascular endothelium-specific ET-1 knockout mice compared with control mice that were homozygous for the floxed allele. In mice pretreated for 3 days with the endothelin A antagonist, ABT-627, or the dual endothelin A/B receptor antagonist, A-182086, the pressor response to CSS was similar between genotypes. CSS significantly increased plasma ET-1 levels in control mice that were homozygous for the floxed allele. CSS failed to elicit an increase in plasma ET-1 in vascular endothelium-specific ET-1 knockout mice. Telemetry frequency domain analyses suggested similar autonomic responses to stress between genotypes, and isolated resistance arteries demonstrated similar sensitivity to α

conclusionsThese findings specify that acute stress-induced activation of endothelium-derived ET-1 and subsequent endothelin A receptor activation is a novel mediator of the blood pressure response to acute psychosocial stress.

Indexed as

VasoconstrictionAdrenergic alpha-1 Receptor AgonistsAnimalsAorta, ThoracicArterial PressureDisease Models, AnimalEndothelin-1Endothelin A Receptor AntagonistsMaleMesenteric ArteriesMice, KnockoutReceptor, Endothelin ASignal TransductionStress, PsychologicalSympathetic Nervous SystemAdrenergic alpha-1 Receptor AgonistsEndothelin-1Endothelin A Receptor AntagonistsReceptor, Endothelin Acage switch stressendothelin‐1endothelium‐derived factorspsychosocial stressstressvascular endothelium‐specific ET‐1 knockout mice

Identifiers

PMID29453306
PMCPMC5850198
OpenAlexW2789905702

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.