Evidence map›Paper›PMID 26580484›Full record

ReviewThe Journal of physiology2016

Compromised blood-brain barrier permeability: novel mechanism by which circulating angiotensin II signals to sympathoexcitatory centres during hypertension.

V C Biancardi, J E Stern

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 115 citations in OpenAlex.

  1. Review
  2. Article
  3. New insights and predictability from in vivo recordings of paroxysmal sympathetic hyperactivity in disorders of consciousness.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2026
    Article
  4. Comparative Study on the Neuroprotective Effects of Perindopril and Benazepril in Experimentally-induced Chronic Mild Stress in Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Physical exercise is essential for increasing ventricular contractility in hypertensive rats treated with losartan.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  15. Article
  16. The Renin Angiotensin System as a Therapeutic Target in Traumatic Brain Injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  17. Article
  18. Review
  19. 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

2 authors at 2 institutions in 1 country.

V C BiancardiDepartment of Physiology, Georgia Regents University, Augusta, GA, USA.
J E SternDepartment of Physiology, Georgia Regents University, Augusta, GA, USA.
Augusta University · USGeorgia Regents Medical Center · US

Funding

CENTRAL NEURONAL-GLIAL MECHANISMS AND NEUROHUMORAL ACTIVATION IN HYPERTENSIONR01HL112225 · NHLBI · GEORGIA STATE UNIVERSITY · PI STERN, JAVIER E · 2012 to 2015
$1.5M
NHLBI NIH HHS HL112225NHLBI NIH HHS R01 HL112225
6 · The paper itself

Abstract

Angiotensin II (AngII) is a pivotal peptide implicated in the regulation of blood pressure. In addition to its systemic vascular and renal effects, AngII acts centrally to modulate the activities of neuroendocrine and sympathetic neuronal networks, influencing in turn sympatho-humoral outflows to the circulation. Moreover, a large body of evidence supports AngII signalling dysregulation as a key mechanism contributing to exacerbated sympathoexcitation during hypertension. Due to its hydrophilic actions, circulating AngII does not cross the blood-brain barrier (BBB), signalling to the brain via the circumventricular organs which lack a tight BBB. In this review, we present and discuss recent studies from our laboratory showing that elevated circulating levels of AngII during hypertension result in disruption of the BBB integrity, allowing access of circulating AngII to critical sympathoexcitatory brain centres such as the paraventricular nucleus of the hypothalamus and the rostral ventrolateral medulla. We propose the novel hypothesis that AngII-driven BBB breakdown constitutes a complementary mechanism by which circulating AngII, working in tandem with the central renin-angiotensin system, further exacerbates sympatho-humoral activation during hypertension. These results are discussed within the context of a growing body of evidence in the literature supporting AngII as a pro-inflammatory signal, and brain microglia as key cell targets mediating central AngII actions during hypertension.

Indexed as

Capillary PermeabilityAngiotensin IIAnimalsBlood-Brain BarrierHumansHypertensionSympathetic Nervous SystemAngiotensin II

Identifiers

PMID26580484
PMCPMC4799983
OpenAlexW2178348782

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.