Evidence map›Paper›PMID 17374517›Full record

ReviewRespiratory physiology & neurobiology2007

Carotid body function in heart failure.

Harold D Schultz, Yu Long Li

Open access · greenAbstract readReview
In one paragraph

Review in Respiratory physiology & neurobiology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

43 citing papers in PubMed, 108 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Regulation of carotid body oxygen sensing by hypoxia-inducible factors.Pflugers Archiv : European journal of physiology · 2016
    Review
  12. Article
  13. Oxygen Sensing and Homeostasis.Physiology (Bethesda, Md.) · 2015
    Review
  14. Article
  15. Humans In Hypoxia: A Conspiracy Of Maladaptation?!Physiology (Bethesda, Md.) · 2015
    Review
  16. TASK channels in arterial chemoreceptors and their role in oxygen and acid sensing.Pflugers Archiv : European journal of physiology · 2015
    Review
  17. Modulation of angiotensin II signaling following exercise training in heart failure.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  18. Effects of exercise training on neurovascular control and skeletal myopathy in systolic heart failure.American journal of physiology. Heart and circulatory physiology · 2015
    Review
  19. Review
  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 1 institution in 2 countries.

Harold D SchultzDepartment of Cellular and Integrative Physiology, University of Nebraska College of Medicine, 985850 Nebraska Medical Center, Omaha, NE 68198-5850, USA. hschultz@unmc.edu
Yu Long Li
Laboratoire d’immunologie intégrative du cancer · FR

Funding

The Role of Excitatory Input into the PVN on Increased Sympathetic Drive in HeartP01HL062222 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI SCHULTZ, HAROLD D · 1999 to 2019
$32.2M
NHLBI NIH HHS P01 HL062222
6 · The paper itself

Abstract

In this review, we summarize the present state of knowledge of the functional characteristics of the carotid body (CB) chemoreflex with respect to control of sympathetic nerve activity (SNA) in chronic heart failure (CHF). Evidence from both CHF patients and animal models of CHF has clearly established that the CB chemoreflex is enhanced in CHF and contributes to the tonic elevation in SNA. This adaptive change derives from altered function at the level of both the afferent and central nervous system (CNS) pathways of the reflex arc. At the level of the CB, an elevation in basal afferent discharge occurs under normoxic conditions in CHF rabbits, and the discharge responsiveness to hypoxia is enhanced. Outward voltage-gated K(+) currents (I(K)) are suppressed in CB glomus cells from CHF rabbits, and their sensitivity to hypoxic inhibition is enhanced. These changes in I(K) derive partly from downregulation of nitric oxide synthase (NOS)/NO signaling and upregulation of angiotensin II (Ang II)/Ang II receptor (AT(1)R) signaling in glomus cells. At the level of the CNS, interactions of the enhanced input from CB chemoreceptors with altered input from baroreceptor and cardiac afferent pathways and from central Ang II further enhance sympathetic drive. In addition, impaired function of NO in the paraventricular nucleus of the hypothalamus participates in the increased SNA response to CB chemoreceptor activation. These results underscore the principle that multiple mechanisms involving Ang II and NO at the level of both the CB and CNS represent complementary and perhaps redundant adaptive mechanisms to enhance CB chemoreflex function in CHF.

Indexed as

Angiotensin IIAnimalsCarotid BodyChemoreceptor CellsHeartHeart FailureHumansHypoxiaNitric OxideParaventricular Hypothalamic NucleusReflexSympathetic Nervous SystemAngiotensin IINitric Oxide

Identifiers

PMID17374517
PMCPMC1965591
OpenAlexW2097433357

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.