Evidence map›Paper›PMID 26838032›Full record

ReviewCurrent hypertension reports2016

Neural Control of Blood Pressure in Chronic Intermittent Hypoxia.

Brent Shell, Katelynn Faulk, J Thomas Cunningham

Abstract readReview
In one paragraph

Review in Current hypertension reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

40 citing papers in PubMed, 59 citations in OpenAlex.

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  5. Review
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  10. Review
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  12. Role of angiotensin II in chronic intermittent hypoxia-induced hypertension and cognitive decline.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    Review
  13. Article
  14. Review
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  18. Review
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  20. Hydrogen peroxide inhibits neurons in the paraventricular nucleus of the hypothalamus via potassium channel activation.American journal of physiology. Regulatory, integrative and comparative physiology · 2019
    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

3 authors at 2 institutions in 1 country.

Brent ShellInstitute for Cardiovascular and Metabolic Diseases, University of North Texas Health Science Center, EAD 332B, 3500 Camp Bowie Blvd, Fort Worth, TX, 76107, USA.
Katelynn FaulkInstitute for Cardiovascular and Metabolic Diseases, University of North Texas Health Science Center, EAD 332B, 3500 Camp Bowie Blvd, Fort Worth, TX, 76107, USA.
J Thomas CunninghamInstitute for Cardiovascular and Metabolic Diseases, University of North Texas Health Science Center, EAD 332B, 3500 Camp Bowie Blvd, Fort Worth, TX, 76107, USA. Tom.Cunningham@unthsc.edu.
University of North Texas Health Science Center · USUniversity of North Texas · US

Funding

Neurohumoral Adaptations to Chronic Intermittent Hypoxia: Insights into the Pathophysiology of Sleep ApneaP01HL088052 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI TONEY, GLENN M · 2008 to 2019
$18.8M
Training in the Neurobiology of Aging and Alzheimer's DiseaseT32AG020494 · NIA · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI ROBERT Clinton BARBER, NATHALIE SUMIEN · 2002 to 2026
$6.9M
Homeostatic Regulation of Supraoptic Neurons: Role of BDNFR01HL119458 · NHLBI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI CUNNINGHAM, J THOMAS · 2014 to 2017
$1.5M
NHLBI NIH HHS P01 HL088052NHLBI NIH HHS R01 HL119458NIA NIH HHS T32 AG020494
6 · The paper itself

Abstract

Sleep apnea (SA) is increasing in prevalence and is commonly comorbid with hypertension. Chronic intermittent hypoxia is used to model the arterial hypoxemia seen in SA, and through this paradigm, the mechanisms that underlie SA-induced hypertension are becoming clear. Cyclic hypoxic exposure during sleep chronically stimulates the carotid chemoreflexes, inducing sensory long-term facilitation, and drives sympathetic outflow from the hindbrain. The elevated sympathetic tone drives hypertension and renal sympathetic activity to the kidneys resulting in increased plasma renin activity and eventually angiotensin II (Ang II) peripherally. Upon waking, when respiration is normalized, the sympathetic activity does not diminish. This is partially because of adaptations leading to overactivation of the hindbrain regions controlling sympathetic outflow such as the nucleus tractus solitarius (NTS), and rostral ventrolateral medulla (RVLM). The sustained sympathetic activity is also due to enhanced synaptic signaling from the forebrain through the paraventricular nucleus (PVN). During the waking hours, when the chemoreceptors are not exposed to hypoxia, the forebrain circumventricular organs (CVOs) are stimulated by peripherally circulating Ang II from the elevated plasma renin activity. The CVOs and median preoptic nucleus chronically activate the PVN due to the Ang II signaling. All together, this leads to elevated nocturnal mean arterial pressure (MAP) as a response to hypoxemia, as well as inappropriately elevated diurnal MAP in response to maladaptations.

Indexed as

Blood PressureAnimalsBrainChronic DiseaseHumansHypertensionHypoxiaSleep Apnea SyndromesChronic intermittent hypoxia (CIH)HypertensionSleep apnea (SA)Sympathetic nerve activity (SNA)

Identifiers

PMID26838032
PMCPMC5080908
OpenAlexW2265626926

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.