ArticleAmerican journal of physiology. Heart and circulatory physiology2016
Bilateral common carotid artery stenosis in normotensive rats impairs endothelium-dependent dilation of parenchymal arterioles.
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.
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.
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.
Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- A male rat model integrating hypertension, chronic cerebral hypoperfusion, and aging recapitulates multimodal cerebral small vessel disease phenotypes.Frontiers in aging neuroscience · 2026Article
- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
- High-fat feeding has sex-dependent effects on the structure and biomechanical properties of cerebral parenchymal arterioles and cognitive function.American journal of physiology. Heart and circulatory physiology · 2025Article
- Endothelial cells as key players in cerebral small vessel disease.Nature reviews. Neuroscience · 2025Review
- Dynamic Neuro-Glial-Vascular Responses in a Mouse Model of Vascular Cognitive Impairment.Neuroglia (Basel, Switzerland) · 2024Article
- Female mice are protected from impaired parenchymal arteriolar TRPV4 function and impaired cognition in hypertension.American journal of physiology. Heart and circulatory physiology · 2023Article
- Chronic cerebral hypoperfusion in male rats results in sustained HPA activation and hyperinsulinemia.American journal of physiology. Endocrinology and metabolism · 2022Article
- Review
- Decreased parenchymal arteriolar tone uncouples vessel-to-neuronal communication in a mouse model of vascular cognitive impairment.GeroScience · 2021Article
- Impaired Glymphatic Function and Pulsation Alterations in a Mouse Model of Vascular Cognitive Impairment.Frontiers in aging neuroscience · 2021Article
- Soluble epoxide hydrolase inhibition improves cognitive function and parenchymal artery dilation in a hypertensive model of chronic cerebral hypoperfusion.Microcirculation (New York, N.Y. : 1994) · 2021Article
- Deficiency in CD4 T Cells Leads to Enhanced Postpartum Internal Carotid Artery Vasoconstriction in Mice: The Role of Nitric Oxide.Frontiers in physiology · 2021Article
- 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 · 2020Article
- Transient receptor potential vanilloid 4 channels are important regulators of parenchymal arteriole dilation and cognitive function.Microcirculation (New York, N.Y. : 1994) · 2019Article
- Transient receptor potential vanilloid-4 channels are involved in diminished myogenic tone in brain parenchymal arterioles in response to chronic hypoperfusion in mice.Acta physiologica (Oxford, England) · 2019Article
- Locus Coeruleus Degeneration Induces Forebrain Vascular Pathology in a Transgenic Rat Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Article
- Gradual common carotid artery occlusion as a novel model for cerebrovascular Hypoperfusion.Metabolic brain disease · 2018Article
- Mineralocorticoid receptor antagonism improves parenchymal arteriole dilation via a TRPV4-dependent mechanism and prevents cognitive dysfunction in hypertension.American journal of physiology. Heart and circulatory physiology · 2018Article
- Carotid artery stenosis in hypertensive rats impairs dilatory pathways in parenchymal arterioles.American journal of physiology. Heart and circulatory physiology · 2018Article
- Total Flavone of Rhododendron Improves Cerebral Ischemia Injury by Activating Vascular TRPV4 to Induce Endothelium-Derived Hyperpolarizing Factor-Mediated Responses.Evidence-based complementary and alternative medicine : eCAM · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
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
Identifiers
What OpenQuestion holds
Registered trials
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.