Evidence map›Paper›PMID 22268114›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2012

Impairment of neurovascular coupling in type 1 diabetes mellitus in rats is linked to PKC modulation of BK(Ca) and Kir channels.

Francesco Vetri, Haoliang Xu, Chanannait Paisansathan, Dale A Pelligrino

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

27 citing papers in PubMed, 43 citations in OpenAlex.

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  11. Differential pial and penetrating arterial responses examined by optogenetic activation of astrocytes and neurons.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
    Article
  12. Article
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  14. The effect of hyperglycemia on neurovascular coupling and cerebrovascular patterning in zebrafish.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  15. The Ion Channel and GPCR Toolkit of Brain Capillary Pericytes.Frontiers in cellular neuroscience · 2020
    Review
  16. Review
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  18. Capillary KNature neuroscience · 2017
    Article
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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

4 authors at 1 institution in 1 country.

Francesco VetriNeuroanesthesia Research Laboratory, Department of Anesthesiology, University of Illinois at Chicago, 60612, USA. vetri@uic.edu
Haoliang Xu
Chanannait Paisansathan
Dale A Pelligrino
University of Illinois Chicago · US

Funding

Astrocytes and neurovascular couplingR01HL088259 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI PELLIGRINO, DALE ALAN · 2008 to 2011
$1.6M
NHLBI NIH HHS HL-088259
6 · The paper itself

Abstract

We hypothesized that chronic hyperglycemia has a detrimental effect on neurovascular coupling in the brain and that this may be linked to protein kinase C (PKC)-mediated phosphorylation. Therefore, in a rat model of streptozotocin-induced chronic type 1 diabetes mellitus (T1DM), and in nondiabetic (ND) controls, we monitored pial arteriole diameter changes during sciatic nerve stimulation and topical applications of the large-conductance Ca(2+)-operated K(+) channel (BK(Ca)) opener, NS-1619, or the K(+) inward rectifier (Kir) channel agonist, K(+). In the T1DM vs. ND rats, the dilatory response associated with sciatic nerve stimulation was decreased by ∼30%, whereas pial arteriolar dilations to NS-1619 and K(+) were largely suppressed. These responses were completely restored by the acute topical application of a PKC antagonist, calphostin C. Moreover, the suffusion of a PKC activator, phorbol 12,13-dibutyrate, in ND rats was able to reproduce the vascular reactivity impairments found in T1DM rats. Assay of PKC activity in brain samples from T1DM vs. ND rats revealed a significant gain in activity only in specimens harvested from the pial and superficial glia limitans tissue, but not in bulk cortical gray matter. Altogether, these findings suggest that the T1DM-associated impairment of neurovascular coupling may be mechanistically linked to a readily reversible PKC-mediated depression of BK(Ca) and Kir channel activity.

Indexed as

Cerebrovascular CirculationVasodilationAnimalsArteriolesBenzimidazolesDiabetes ComplicationsDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Electric StimulationEnzyme ActivationEnzyme ActivatorsFemaleLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsNaphthalenesPhorbol 12,13-DibutyratePhosphorylationBenzimidazolescalphostin CEnzyme ActivatorsKcnma1 protein, ratLarge-Conductance Calcium-Activated Potassium Channel alpha SubunitsNaphthalenesNS 1619Phorbol 12,13-DibutyratePotassiumPotassium ChannelsPotassium Channels, Inwardly RectifyingProtein Kinase CProtein Kinase Inhibitors

Identifiers

PMID22268114
PMCPMC3311480
OpenAlexW2123108580

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.