Evidence map›Paper›PMID 21078591›Full record

ArticleThe Journal of physiology2011

Role of blood flow in carotid body chemoreflex function in heart failure.

Yanfeng Ding, Yu-Long Li, Harold D Schultz

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing 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

77 citing papers in PubMed, 129 citations in OpenAlex.

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  5. Obligatory neural feedback control of exercise cardiorespiratory function and performance.Journal of applied physiology (Bethesda, Md. : 1985) · 2025
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  16. Autonomic cardiovascular control during exercise.American journal of physiology. Heart and circulatory physiology · 2023
    Review
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  20. Review

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 2 countries.

Yanfeng DingDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE 68198-5850, USA.
Yu-Long Li
Harold D Schultz
University of Nebraska Medical Center · USUniversity of Nebraska–Lincoln · US

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
Dysfunction of Baroreceptor Neurons in Heart Failure: Cellular and Molecular MechR01HL098503 · NHLBI · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI LI, YU-LONG · 2010 to 2013
$1.5M
NHLBI NIH HHS P01 HL062222NHLBI NIH HHS P01-HL62222NHLBI NIH HHS R01 HL098503
6 · The paper itself

Abstract

Peripheral chemoreflex sensitivity is potentiated in clinical and experimental chronic heart failure (CHF). Blood supply to tissues is inevitably reduced in CHF. However, it remains poorly understood whether the reduced blood flow is the cause of increased peripheral chemoreflex sensitivity in CHF. This work highlights the effect of chronically reduced blood flow to the carotid body (CB) on peripheral chemoreflex function in rabbits. In pacing-induced CHF rabbits, blood flow in the carotid artery was reduced by 36.4 ± 5.2% after 3 weeks of pacing. For comparison, a similar level of blood flow reduction was induced by carotid artery occlusion (CAO) over a similar 3 week time course without pacing. CB blood supply was reduced by similar levels in both CHF and CAO rabbits as measured with fluorescent microspheres. Compared with sham rabbits, CAO enhanced peripheral chemoreflex sensitivity in vivo, increased CB chemoreceptor activity in an isolated CB preparation and decreased outward potassium current (Ik) in CB glomus cells to levels similar to those that were observed in CHF rabbits. In CAO CB compared to sham, neural nitric oxide (NO) synthase (nNOS) expression and NO levels were suppressed, and angiotensin II (Ang II) type 1 receptor (AT1-R) protein expression and Ang II concentration were elevated; these changes were similar to those seen in the CB from CHF rabbits. A NO donor and AT1-R antagonist reversed CAO-enhanced chemoreflex sensitivity. These results suggest that a reduction of blood flow to the CB is involved in the augmentation of peripheral chemoreflex sensitivity in CHF.

Indexed as

ReflexAngiotensin IIAngiotensin II Type 1 Receptor BlockersAnimalsBlood Flow VelocityCardiac Pacing, ArtificialCarotid ArteriesCarotid BodyChemoreceptor CellsConstrictionDisease Models, AnimalHeart FailureKidneyMaleNitric OxideNitric Oxide DonorsAngiotensin IIAngiotensin II Type 1 Receptor BlockersNitric OxideNitric Oxide DonorsNitric Oxide Synthase Type IPotassiumReceptor, Angiotensin, Type 1

Identifiers

PMID21078591
PMCPMC3039273
OpenAlexW2071011552

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.