Evidence map›Paper›PMID 26968546›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2016

Bilateral common carotid artery stenosis in normotensive rats impairs endothelium-dependent dilation of parenchymal arterioles.

Nusrat Matin, Courtney Fisher, William F Jackson, Anne M Dorrance

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

22 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Review
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  7. Chronic cerebral hypoperfusion in male rats results in sustained HPA activation and hyperinsulinemia.American journal of physiology. Endocrinology and metabolism · 2022
    Article
  8. Review
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  13. Sex-specific effects of high-fat diet on cognitive impairment in a mouse model of VCID.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  14. Article
  15. Article
  16. Article
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  19. Carotid artery stenosis in hypertensive rats impairs dilatory pathways in parenchymal arterioles.American journal of physiology. Heart and circulatory physiology · 2018
    Article
  20. 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

4 authors at 1 institution in 1 country.

Nusrat MatinDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan matinnus@msu.edu.
Courtney FisherDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
William F JacksonDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Anne M DorranceDepartment of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan.
Michigan State University · US

Funding

SIGNALING MECHANISMS IN ARTERIES AND VEINS IN HYPERTENSIONP01HL070687 · NHLBI · MICHIGAN STATE UNIVERSITY · PI WATTS, STEPHANIE W · 2003 to 2019
$22.8M
Integrative Training in the Pharmacological SciencesT32GM092715 · NIGMS · MICHIGAN STATE UNIVERSITY · PI NEUBIG, RICHARD R · 2011 to 2020
$1.5M
NHLBI NIH HHS P01 HL070687NIGMS NIH HHS T32 GM092715
6 · The paper itself

Abstract

Chronic cerebral hypoperfusion is a risk factor for cognitive impairment. Reduced blood flow through the common carotid arteries induced by bilateral carotid artery stenosis (BCAS) is a physiologically relevant model of chronic cerebral hypoperfusion. We hypothesized that BCAS in 20-wk-old Wistar-Kyoto (WKY) rats would impair cognitive function and lead to reduced endothelium-dependent dilation and outward remodeling in the parenchymal arterioles (PAs). After 8 wk of BCAS, both short-term memory and spatial discrimination abilities were impaired. In vivo assessment of cerebrovascular reserve capacity showed a severe impairment after BCAS. PA endothelial function and structure were assessed by pressure myography. BCAS impaired endothelial function in PAs, as evidenced by reduced dilation to carbachol. Addition of nitric oxide synthase and cyclooxygenase inhibitors did not change carbachol-mediated dilation in either group. Inhibiting CYP epoxygenase, the enzyme that produces epoxyeicosatrienoic acid (EETs), a key determinant of endothelium-derived hyperpolarizing factor (EDHF)-mediated dilation, abolished dilation in PAs from Sham rats, but had no effect in PAs from BCAS rats. Expression of TRPV4 channels, a target for EETs, was decreased and maximal dilation to a TRPV4 agonist was attenuated after BCAS. Together these data suggest that EET-mediated dilation is impaired in PAs after BCAS. Thus impaired endothelium-dependent dilation in the PAs may be one of the contributing factors to the cognitive impairment observed after BCAS.

Indexed as

VasodilationAnimalsArteriolesBehavior, AnimalBrainCarotid Artery, CommonCarotid StenosisCerebrovascular CirculationCerebrovascular DisordersCognitionCognition DisordersDisease Models, AnimalEicosanoidsEndothelium, VascularLigationMemory, Short-TermEicosanoidsTrpv4 protein, ratTRPV Cation Channelscerebral microcirculationendothelium-dependent dilationepoxyeicosatrienoic acidparenchymal arteriolesposterior communicating arteryvascular remodeling

Identifiers

PMID26968546
PMCPMC4895832
OpenAlexW2294201386

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.