Evidence map›Paper›PMID 19427376›Full record

ArticleBrain, behavior, and immunity2009

In vivo Angiotensin II AT1 receptor blockade selectively inhibits LPS-induced innate immune response and ACTH release in rat pituitary gland.

Enrique Sánchez-Lemus, Julius Benicky, Jaroslav Pavel, Juan M Saavedra

Open access · greenAbstract read
In one paragraph

Article in Brain, behavior, and immunity, 2009. 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
1.8field-weighted citation impact, top 15% 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, 45 citations in OpenAlex.

  1. Article
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  4. Neuroendocrine-Immune Regulatory Network ofMolecules (Basel, Switzerland) · 2022
    Review
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  10. Review
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  15. Angiotensin II AT1 receptor blockade ameliorates brain inflammation.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2011
    Article
  16. Review
  17. 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

4 authors at 2 institutions in 1 country.

Enrique Sánchez-LemusSection on Pharmacology, Division of Intramural Research Programs, Department of Health and Human Services, National Institute of Mental Health, National Institutes of Health, Bethesda, MD 20892, USA. sancheze@mail.nih.gov
Julius Benicky
Jaroslav Pavel
Juan M Saavedra
National Institutes of Health · USNational Institute of Mental 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 Z01 MH002762
6 · The paper itself

Abstract

Systemic lipopolysaccharide (LPS) administration induces an innate immune response and stimulates the hypothalamic-pituitary-adrenal axis. We studied Angiotensin II AT(1) receptor participation in the LPS effects with focus on the pituitary gland. LPS (50 microg/kg, i.p.) enhanced, 3h after administration, gene expression of pituitary CD14 and that of Angiotensin II AT(1A) receptors in pituitary and hypothalamic paraventricular nucleus (PVN); stimulated ACTH and corticosterone release; decreased pituitary CRF(1) receptor mRNA and increased all plasma and pituitary pro-inflammatory factors studied. The AT(1) receptor blocker (ARB) candesartan (1mg/kg/day, s.c. daily for 3 days before LPS) blocked pituitary and PVN AT(1) receptors, inhibited LPS-induced ACTH but not corticosterone secretion and decreased LPS-induced release of TNF-alpha, IL-1beta and IL-6 to the circulation. The ARB reduced LPS-induced pituitary gene expression of IL-6, LIF, iNOS, COX-2 and IkappaB-alpha; and prevented LPS-induced increase of nNOS/eNOS activity. The ARB did not affect LPS-induced TNF-alpha and IL-1beta gene expression, IL-6 or IL-1beta protein content or LPS-induced decrease of CRF(1) receptors. When administered alone, the ARB increased basal plasma corticosterone levels and basal PGE(2) mRNA in pituitary. Our results demonstrate that the pituitary gland is a target for systemically administered LPS. AT(1) receptor activity is necessary for the complete pituitary response to LPS and is limited to specific pro-inflammatory pathways. There is a complementary and complex influence of the PVN and circulating cytokines on the initial pituitary response to LPS. Our findings support the proposal that ARBs may be considered for the treatment of inflammatory conditions.

Indexed as

Adrenocorticotropic HormoneAnalysis of VarianceAngiotensin II Type 1 Receptor BlockersAnimalsAutoradiographyBenzimidazolesBiphenyl CompoundsCorticosteroneCytokinesDinoprostoneEnzyme-Linked Immunosorbent AssayHypothalamo-Hypophyseal SystemInflammationIn Situ HybridizationLipopolysaccharidesMaleAdrenocorticotropic HormoneAngiotensin II Type 1 Receptor BlockersBenzimidazolesBiphenyl CompoundscandesartanCorticosteroneCytokinesDinoprostoneLipopolysaccharidesReceptor, Angiotensin, Type 1RNA, MessengerTetrazoles

Identifiers

PMID19427376
PMCPMC2749886
OpenAlexW1993516207

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.