Evidence map›Paper›PMID 28842441›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2018

Carotid artery stenosis in hypertensive rats impairs dilatory pathways in parenchymal arterioles.

Nusrat Matin, Courtney Fisher, William F Jackson, Janice M Diaz-Otero, Anne M Dorrance

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.5field-weighted citation impact, top 29% 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

8 citing papers in PubMed, 15 citations in OpenAlex.

  1. Cumulative blood pressure exposure and cognition: the potential mediating role of brain volume.Hypertension research : official journal of the Japanese Society of Hypertension · 2026
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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

5 authors at 1 institution in 1 country.

Nusrat MatinDepartment of Pharmacology and Toxicology, Michigan State University , East Lansing, Michigan.
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.
Janice M Diaz-OteroDepartment 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
Cerebral parenchymal arteriole dysfunction and cognitive decline in a life-long high fat feeding modelR01HL137694 · NHLBI · MICHIGAN STATE UNIVERSITY · PI DORRANCE, ANNE M., JACKSON, WILLIAM F. · 2017 to 2020
$2.1M
Integrative Training in the Pharmacological SciencesT32GM092715 · NIGMS · MICHIGAN STATE UNIVERSITY · PI NEUBIG, RICHARD R · 2011 to 2020
$1.5M
NHLBI NIH HHS P01 HL070687NHLBI NIH HHS R01 HL137694NIGMS NIH HHS T32 GM092715
6 · The paper itself

Abstract

Hypertension is a leading risk factor for vascular cognitive impairment and is strongly associated with carotid artery stenosis. In normotensive rats, chronic cerebral hypoperfusion induced by bilateral common carotid artery stenosis (BCAS) leads to cognitive impairment that is associated with impaired endothelium-dependent dilation in parenchymal arterioles (PAs). The aim of this study was to assess the effects of BCAS on PA function and structure in stroke-prone spontaneously hypertensive rats, a model of human essential hypertension. Understanding the effects of hypoperfusion on PAs in a hypertensive model could lead to the identification of therapeutic targets for cognitive decline in a model that reflects the at-risk population. We hypothesized that BCAS would impair endothelium-dependent dilation in PAs and induce artery remodeling compared with sham rats. PAs from BCAS rats had endothelial dysfunction, as assessed using pressure myography. Inhibition of nitric oxide and prostaglandin production had no effect on PA dilation in sham or BCAS rats. Surprisingly, inhibition of epoxyeicosatrienoic acid production increased dilation in PAs from BCAS rats but not from sham rats. Similar results were observed in the presence of inhibitors for all three dilatory pathways, suggesting that epoxygenase inhibition may have restored a nitric oxide/prostaglandin-independent dilatory pathway in PAs from BCAS rats. PAs from BCAS rats underwent remodeling with a reduced wall thickness. These data suggest that marked endothelial dysfunction in PAs from stroke-prone spontaneously hypertensive rats with BCAS may be associated with the development of vascular cognitive impairment. NEW & NOTEWORTHY The present study assessed the structure and function of parenchymal arterioles in a model of chronic cerebral hypoperfusion and hypertension, both of which are risk factors for cognitive impairment. We observed that impaired dilation and artery remodeling in parenchymal arterioles and abolished cerebrovascular reserve capacity may mediate cognitive deficits.

Indexed as

Cerebrovascular CirculationVasodilationAnimalsArteriolesBehavior, AnimalBrainCarotid Artery, CommonCarotid StenosisCerebrovascular DisordersCognitionCognition DisordersDisease Models, AnimalHypertensionMaleMemoryParenchymal Tissuecarotid stenosiscerebral arteriescognitive impairmentdilationhypertensionparenchymal arterioles

Identifiers

PMID28842441
PMCPMC5866397
OpenAlexW2747497136

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.