Evidence map›Paper›PMID 21684261›Full record

ArticleBiochemical pharmacology2011

Endothelial cell-specific aryl hydrocarbon receptor knockout mice exhibit hypotension mediated, in part, by an attenuated angiotensin II responsiveness.

Larry N Agbor, Khalid M Elased, Mary K Walker

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemical pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 21% 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, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. AHR in the intestinal microenvironment: safeguarding barrier function.Nature reviews. Gastroenterology & hepatology · 2021
    Review
  11. Review
  12. Article
  13. Article
  14. Article
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  16. Article
  17. Review
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  19. Association of Dioxin and Dioxin-like Congeners With Hypertension.Federal practitioner : for the health care professionals of the VA, DoD, and PHS · 2018
    Article
  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

3 authors at 2 institutions in 1 country.

Larry N AgborDepartment of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico, Health Sciences Center, Albuquerque, NM, USA.
Khalid M Elased
Mary K Walker
University of New Mexico · USWright State University · US

Funding

Ah Receptor and Endothelin-Dependent HypertensionR01HL078914 · NHLBI · UNIVERSITY OF NEW MEXICO · PI WALKER, MARY K · 2006 to 2010
$1.9M
NHLBI NIH HHS R01 HL078914
6 · The paper itself

Abstract

Hypotension in aryl hydrocarbon receptor knockout mice (ahr(-/-)) is mediated, in part, by a reduced contribution of angiotensin (Ang) II to basal blood pressure (BP). Since AHR is highly expressed in endothelial cells (EC), we hypothesized that EC-specific ahr(-/-) (ECahr(-/-)) mice would exhibit a similar phenotype. We generated ECahr(-/-) mice by crossing AHR floxed mice (ahr(fx/fx)) to mice expressing Cre recombinase driven by an EC-specific promoter. BP was assessed by radiotelemetry prior to and following an acute injection of Ang II or chronic treatment with an angiotensin converting enzyme inhibitor (ACEi). ECahr(-/-) mice were hypotensive (ECahr(+/+): 116.1±1.4; ECahr(-/-): 107.4±2.0 mmHg, n=11, p<0.05) and exhibited significantly different responses to Ang II and ACEi. While Ang II increased BP in both genotypes, the increase was sustained in ECahr(+/+), whereas the increase in ECahr(-/-) mice steadily declined. Area under the curve analysis showed that Ang II-induced increase in diastolic BP (DBP) over 30 min was significantly lower in ECahr(-/-) mice (ECahr(+/+) 1297±223 mmHg/30 min; ECahr(-/-)(AUC): 504±138 mmHg/30 min, p<0.05). In contrast, while ACEi decreased BP in both genotypes, the subsequent rise in DBP after treatment was significantly delayed in the ECahr(-/-) mice. ECahr(-/-) mice also exhibited reduced vascular and adipose Ang II type 1 receptor (AT1R) expression, and reduced aortic Ang II-dependent vasoconstriction in the presence of vascular adipose. Taken together these data suggest that hypotension in ECahr(-/-) mice results from reduced vascular responsiveness to Ang II that is influenced by AT1R expression and adipose.

Indexed as

Angiotensin IIAnimalsBasic Helix-Loop-Helix ProteinsBlood PressureEndothelial CellsFemaleHeart RateHypotensionMaleMiceMice, KnockoutNitric Oxide SynthaseOrgan SizeReceptor, Angiotensin, Type 1Receptors, Aryl HydrocarbonRenin-Angiotensin SystemAhr protein, mouseAngiotensin IIBasic Helix-Loop-Helix ProteinsNitric Oxide SynthaseReceptor, Angiotensin, Type 1Receptors, Aryl HydrocarbonRNA, Messenger

Identifiers

PMID21684261
PMCPMC3148414
OpenAlexW2010664466

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

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.