Evidence map›Paper›PMID 18556352›Full record

ArticleEndocrinology2008

Angiotensin II AT1 receptor blockade decreases lipopolysaccharide-induced inflammation in the rat adrenal gland.

Enrique Sanchez-Lemus, Yuki Murakami, Ignacio M Larrayoz-Roldan, Armen J Moughamian, Jaroslav Pavel, Tsuyoshi Nishioku, Juan M Saavedra

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

27 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  13. Anti-inflammatory effects of fimasartan via Akt, ERK, and NFκB pathways on astrocytes stimulated by hemolysate.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016
    Article
  14. Effects of angiotensin II type 1 receptor antagonist on rats with septic shock.International journal of clinical and experimental medicine · 2015
    Article
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  17. Review
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  20. Angiotensin II AT1 receptor blockade ameliorates brain inflammation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    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

7 authors at 2 institutions in 1 country.

Enrique Sanchez-LemusSection on Pharmacology, National Institute of Mental Health, National Institutes of Health, Department of Health and Human Services, 10 Center Drive, MSC 1514, Building, 10, Room 2D57, Bethesda, Maryland 20892, USA. sancheze@mail.nih.gov
Yuki Murakami
Ignacio M Larrayoz-Roldan
Armen J Moughamian
Jaroslav Pavel
Tsuyoshi Nishioku
Juan M Saavedra
National Institute of Mental Health · USNational Institutes of Health · US

Funding

Role Of Neuropeptides And Biogenic Amines In Stress and Brain InflammationZIAMH002762 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI SAAVEDRA, JUAN M · 2009 to 2013
$5.2M
ROLE OF NEUROPEPTIDES AND BIOGENIC AMINES IN STRESS AND BRAIN ISCHEMIAZ01MH002762 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI SAAVEDRA, JUAN M · 1997 to 2008
$4.6M
Intramural NIH HHS
6 · The paper itself

Abstract

Peripheral administration of bacterial endotoxin [lipopolysaccharide (LPS)] to rodents produces an innate immune response and hypothalamic-pituitary-adrenal axis stimulation. Renin-angiotensin-aldosterone system inhibition by angiotensin II AT1 receptor blockade has antiinflammatory effects in the vasculature. We studied whether angiotensin II receptor blockers (ARBs) prevent the LPS response. We focused on the adrenal gland, one organ responsive to LPS and expressing a local renin-angiotensin-aldosterone system. LPS (50 microg/kg, ip) produced a generalized inflammatory response with increased release of TNF-alpha and IL-6 to the circulation, enhanced adrenal aldosterone synthesis and release, and enhanced adrenal cyclooxygenase-2, IL-6, and TNF-alpha gene expression. ACTH and corticosterone release were also increased by LPS. Pretreatment with the ARB candesartan (1 mg/kg.d, sc for 3 d before the LPS administration) decreased LPS-induced cytokine release to the circulation, adrenal aldosterone synthesis and release, and cyclooxygenase-2 and IL-6 gene expression. Candesartan did not prevent the LPS-induced ACTH and corticosterone release. Our results suggest that AT1 receptors are essential for the development of the full innate immune and stress responses to bacterial endotoxin. The ARB decreased the general peripheral inflammatory response to LPS, partially decreased the inflammatory response in the adrenal gland, prevented the release of the pro-inflammatory hormone aldosterone, and protected the antiinflammatory effects of glucocorticoid release. An unrestricted innate immune response to the bacterial endotoxin may have deleterious effects for the organism and may lead to development of chronic inflammatory disease. We postulate that the ARBs may have therapeutic effects on inflammatory conditions.

Indexed as

Adrenal GlandsAdrenocorticotropic HormoneAldosteroneAngiotensin II Type 1 Receptor BlockersAnimalsBenzimidazolesBiomarkersBiphenyl CompoundsBlood PressureCorticosteroneInflammationInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesMaleRatsAdrenocorticotropic HormoneAldosteroneAngiotensin II Type 1 Receptor BlockersBenzimidazolesBiomarkersBiphenyl CompoundscandesartanCorticosteroneInterleukin-6Lipopolysaccharide ReceptorsLipopolysaccharidesReceptor, Angiotensin, Type 1TetrazolesTumor Necrosis Factor-alpha

Identifiers

PMID18556352
PMCPMC2582913
OpenAlexW2078034806

What OpenQuestion holds

Textmetadata
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.