Evidence map›Paper›PMID 22984245›Full record

ReviewJournal of applied physiology (Bethesda, Md. : 1985)2012

The brain renin-angiotensin system and cardiovascular responses to stress: insights from transgenic rats with low brain angiotensinogen.

Amy C Arnold, Atsushi Sakima, Sherry O Kasper, Sherry Vinsant, Maria Antonia Garcia-Espinosa, Debra I Diz

Abstract readReview
In one paragraph

Review in Journal of applied physiology (Bethesda, Md. : 1985), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 23 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. No Brain Renin-Angiotensin System: Déjà vu All Over Again?Hypertension (Dallas, Tex. : 1979) · 2017
    Article
  10. Macrophages in neuroinflammation: role of the renin-angiotensin-system.Pflugers Archiv : European journal of physiology · 2017
    Review
  11. 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

6 authors at 1 institution in 1 country.

Amy C ArnoldThe Hypertension & Vascular Research Center and the Departments of General Surgery and Physiology and Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC 27157-1032, USA.
Atsushi Sakima
Sherry O Kasper
Sherry Vinsant
Maria Antonia Garcia-Espinosa
Debra I Diz
Wake Forest University · US

Funding

Vaso-Hormonal Mechanisms in HypertensionP01HL051952 · NHLBI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI GROBAN, LEANNE · 1994 to 2019
$34.8M
Training Program in Translational Radiation OncologyT32CA113267 · NCI · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BLACKSTOCK, ARTHUR W · 2005 to 2014
$2.6M
NCI NIH HHS 2T32CA113267NHLBI NIH HHS HL-051952
6 · The paper itself

Abstract

The renin-angiotensin system (RAS) has been identified as an attractive target for the treatment of stress-induced cardiovascular disorders. The effects of angiotensin (ANG) peptides during stress responses likely result from an integration of actions by circulating peptides and brain peptides derived from neuronal and glial sources. The present review focuses on the contribution of endogenous brain ANG peptides to pathways involved in cardiovascular responses to stressors. During a variety of forms of stress, neuronal pathways in forebrain areas containing ANG II or ANG-(1-7) are activated to stimulate descending angiotensinergic pathways that increase sympathetic outflow to increase blood pressure. We provide evidence that glia-derived ANG peptides influence brain AT(1) receptors. This appears to result in modulation of the responsiveness of the neuronal pathways activated during stressors that elevate circulating ANG peptides to activate brain pathways involving descending hypothalamic projections. It is well established that increased cardiovascular reactivity to stress is a significant predictor of hypertension and other cardiovascular diseases. This review highlights the importance of understanding the impact of RAS components from the circulation, neurons, and glia on the integration of cardiovascular responses to stressors.

Indexed as

Adaptation, PhysiologicalAngiotensinogenAnimalsHeartNeurogliaRatsRats, TransgenicRenin-Angiotensin SystemStress, PhysiologicalAngiotensinogen

Identifiers

PMID22984245
PMCPMC3544491
OpenAlexW2033446773

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.