Evidence map›Paper›PMID 24343120›Full record

ArticleHypertension (Dallas, Tex. : 1979)2014

Circulating angiotensin II gains access to the hypothalamus and brain stem during hypertension via breakdown of the blood-brain barrier.

Vinicia Campana Biancardi, Sook Jin Son, Sahra Ahmadi, Jessica A Filosa, Javier E Stern

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 154 papers.

0numbers the graph read from it
0cells of the map it votes in
154citing papers in PubMed
9.7field-weighted citation impact, top 1% 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

154 citing papers in PubMed, 270 citations in OpenAlex.

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  6. Neuroimmune interactions in cardiovascular homeostasis and disease.American journal of physiology. Cell physiology · 2026
    Review
  7. 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
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94 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Vinicia Campana BiancardiDepartment of Physiology, Georgia Regents University, 1120 15th Street, Augusta, GA 30912. jstern@gru.edu.
Sook Jin Son
Sahra Ahmadi
Jessica A Filosa
Javier E Stern
Georgia Regents Medical Center · US

Funding

Signals and targets underlying mechanisms for neurovascular coupling in the brainR01HL089067 · NHLBI · UNIVERSITY OF CINCINNATI · PI FILOSA, JESSICA A · 2007 to 2017
$3.2M
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 R01 HL089067NHLBI NIH HHS R01HL089067NHLBI NIH HHS R01 HL112225
6 · The paper itself

Abstract

Angiotensin II-mediated vascular brain inflammation emerged as a novel pathophysiological mechanism in neurogenic hypertension. However, the precise underlying mechanisms and functional consequences in relation to blood-brain barrier (BBB) integrity and central angiotensin II actions mediating neurohumoral activation in hypertension are poorly understood. Here, we aimed to determine whether BBB permeability within critical hypothalamic and brain stem regions involved in neurohumoral regulation was altered during hypertension. Using digital imaging quantification after intravascularly injected fluorescent dyes and immunohistochemistry, we found increased BBB permeability, along with altered key BBB protein constituents, in spontaneously hypertensive rats within the hypothalamic paraventricular nucleus, the nucleus of the solitary tract, and the rostral ventrolateral medulla, all critical brain regions known to contribute to neurohumoral activation during hypertension. BBB disruption, including increased permeability and downregulation of constituent proteins, was prevented in spontaneously hypertensive rats treated with the AT1 receptor antagonist losartan, but not with hydralazine, a direct vasodilator. Importantly, we found circulating angiotensin II to extravasate into these brain regions, colocalizing with neurons and microglial cells. Taken together, our studies reveal a novel angiotensin II-mediated feed-forward mechanism during hypertension, by which circulating angiotensin II evokes increased BBB permeability, facilitating in turn its access to critical brain regions known to participate in blood pressure regulation.

Indexed as

Blood PressureAngiotensin IIAnimalsBlood-Brain BarrierBrain StemDisease Models, AnimalHypertensionHypothalamusMaleRatsRats, Inbred SHRRats, Inbred WKYRats, WistarAngiotensin IIangiotensin IIblood–brain barrierbrain stemhypertensionhypothalamusreceptor, angiotensin, type 1

Identifiers

PMID24343120
PMCPMC4080808
OpenAlexW2117536760

What OpenQuestion holds

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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.