Evidence map›Paper›PMID 21659825›Full record

ArticleJournal of hypertension2011

Knockout of the vascular endothelial glucocorticoid receptor abrogates dexamethasone-induced hypertension.

Julie E Goodwin, Junhui Zhang, David Gonzalez, Sebastian Albinsson, David S Geller

Abstract read
In one paragraph

Article in Journal of hypertension, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.3field-weighted citation impact, top 25% 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

25 citing papers in PubMed, 54 citations in OpenAlex.

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  13. Rosiglitazone, a Ligand to PPARPPAR research · 2019
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  19. Endothelial glucocorticoid receptor suppresses atherogenesis--brief report.Arteriosclerosis, thrombosis, and vascular biology · 2015
    Article
  20. 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

5 authors at 5 institutions in 2 countries.

Julie E GoodwinSection of Nephrology, Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520-8064, USA. julie.goodwin@yale.edu
Junhui Zhang
David Gonzalez
Sebastian Albinsson
David S Geller
GTx (United States) · USLund University · SEPediatrics and Genetics · USVeterans Health Administration · USYale University · US

Funding

Yale Mouse Metabolic Phenotyping CenterU24DK059635 · NIDDK · YALE UNIVERSITY · PI SHULMAN, GERALD I · 2001 to 2015
$8.9M
Yale Rheumatic Diseases Research Core CenterP30AR053495 · NIAMS · YALE UNIVERSITY · PI HABERMAN, ANN M · 2007 to 2017
$7.0M
The Role of Vascular Smooth Muscle GR in Acute Glucocorticoid-mediated HTNK08DK078623 · NIDDK · YALE UNIVERSITY · PI GOODWIN, JULIE · 2008 to 2012
$807k
NIAMS NIH HHS P30 AR053495NIAMS NIH HHS P30AR053495NIDDK NIH HHS K08 DK078623NIDDK NIH HHS K08-DK078623NIDDK NIH HHS U24 DK059635NIDDK NIH HHS U24 DK59635
6 · The paper itself

Abstract

backgroundGlucocorticoid-mediated hypertension is incompletely understood. Recent studies have suggested the primary mechanism of this form of hypertension may be through the effects of glucocorticoids on vascular tissues and not to excess sodium and water re-absorption as traditionally believed.

objectiveThe goal of this study was to better understand the role of the vasculature in the generation and maintenance of glucocorticoid-mediated hypertension.

methodsWe created a mouse model with a tissue-specific knockout of the glucocorticoid receptor in the vascular endothelium.

resultsWe show that these mice are relatively resistant to dexamethasone-induced hypertension. After 1 week of dexamethasone treatment, control animals have a mean blood pressure (BP) increase of 13.1 mmHg, whereas knockout animals have only a 2.7 mmHg increase (P < 0.001). Interestingly, the knockout mice have slightly elevated baseline BP compared with the controls (112.2 ± 2.5 vs. 104.6 ± 1.2 mmHg, P = 0.04), a finding which is not entirely explained by our data. Furthermore, we demonstrate that the knockout resistance arterioles have a decreased contractile response to dexamethasone with only 6.6% contraction in knockout vessels compared with 13.4% contraction in control vessels (P = 0.034). Finally, we show that in contrast to control animals, the knockout animals are able to recover a significant portion of their normal circadian BP rhythm, suggesting that the vascular endothelial glucocorticoid receptor may function as a peripheral circadian clock.

conclusionOur study highlights the importance of the vascular endothelial glucocorticoid receptor in several fundamental physiologic processes, namely BP homeostasis and circadian rhythm.

Indexed as

AnimalsBase SequenceBlood PressureDexamethasoneDisease Models, AnimalDNA PrimersEndothelium, VascularHeart RateHypertensionMiceMice, KnockoutReceptors, GlucocorticoidDexamethasoneDNA PrimersReceptors, Glucocorticoid

Identifiers

PMID21659825
PMCPMC3439131
OpenAlexW2012364005

What OpenQuestion holds

Textmetadata
LicenceTDM
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.