Evidence map›Paper›PMID 22723632›Full record

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

Sympatho-adrenal activation by chronic intermittent hypoxia.

Nanduri R Prabhakar, Ganesh K Kumar, Ying-Jie Peng

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 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
4.7field-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

62 citing papers in PubMed, 103 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. P300/CBP Regulates HIF-1-Dependent Sympathetic Activation and Hypertension by Intermittent Hypoxia.American journal of respiratory cell and molecular biology · 2024
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  14. Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. Article
  20. Review

2 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

3 authors at 2 institutions in 1 country.

Nanduri R PrabhakarInstitute for Integrative Physiology and The Center for Systems Biology of Oxygen Sensing, Biological Sciences Division, Dept. of Medicine, University of Chicago, 5841 S. Maryland Ave., Chicago, IL 60637, USA. nanduri@uchicago.edu
Ganesh K Kumar
Ying-Jie Peng
Center for Systems Biology · USUniversity of Chicago · US

Funding

Integrative Consequences of HypoxiaP01HL090554 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2008 to 2017
$21.4M
Consequences of Neonatal HypoxiaR01HL076537 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2005 to 2009
$1.8M
Transmitters in Altered Carotid Body FunctionR01HL086493 · NHLBI · UNIVERSITY OF CHICAGO · PI PRABHAKAR, NANDURI R · 2008 to 2012
$1.8M
NHLBI NIH HHS HL-76537NHLBI NIH HHS HL-86493NHLBI NIH HHS HL-90554
6 · The paper itself

Abstract

Recurrent apnea with chronic intermittent hypoxia (CIH) is a major clinical problem in adult humans and infants born preterm. Patients with recurrent apnea exhibit heightened sympathetic activity as well as elevated plasma catecholamine levels, and these phenotypes are effectively recapitulated in rodent models of CIH. This article summarizes findings from studies addressing sympathetic activation in recurrent apnea patients and rodent models of CIH and the underlying cellular and molecular mechanisms. Available evidence suggests that augmented chemoreflex and attenuated baroreflex contribute to sympathetic activation by CIH. Studies on rodents showed that CIH augments the carotid body response to hypoxia and attenuates the carotid baroreceptor response to increased sinus pressures. Processing of afferent information from chemoreceptors at the central nervous system is also facilitated by CIH. Adult and neonatal rats exposed to CIH exhibit augmented catecholamine secretion from the adrenal medulla. Adrenal demedullation prevents the elevation of circulating catecholamines in CIH-exposed rodents. Reactive oxygen species (ROS)-mediated signaling is emerging as the major cellular mechanism triggering sympatho-adrenal activation by CIH. Molecular mechanisms underlying increased ROS generation by CIH seem to involve transcriptional dysregulation of genes encoding pro-and antioxidant enzymes by hypoxia-inducible factor-1 and -2, respectively.

Indexed as

Adrenal MedullaAnimalsApneaHumansHypoxiaSympathetic Nervous System

Identifiers

PMID22723632
PMCPMC3472486
OpenAlexW2070651032

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.