Evidence map›Paper›PMID 25641345›Full record

ReviewMicrocirculation (New York, N.Y. : 1994)2015

Vascular inward rectifier K+ channels as external K+ sensors in the control of cerebral blood flow.

Thomas A Longden, Mark T Nelson

Open access · greenAbstract readReview
In one paragraph

Review in Microcirculation (New York, N.Y. : 1994), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed
5.4field-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

100 citing papers in PubMed, 151 citations in OpenAlex.

  1. Review
  2. Review
  3. A pericyte chloride clamp mechanism governs capillary control of cerebral blood flow.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Cerebral capillary computation.American journal of physiology. Cell physiology · 2026
    Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Pericyte Electrical Signalling and Brain Haemodynamics.Basic & clinical pharmacology & toxicology · 2025
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article

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

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

2 authors at 1 institution in 2 countries.

Thomas A LongdenDepartment of Pharmacology, College of Medicine, University of Vermont, Burlington, Vermont, USA.
Mark T Nelson
University of Vermont · US

Funding

Proteomics Core for Neuroscience P20 RR16435P20RR016435 · NCRR · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI SPEES, JEFFREY L · 2001 to 2010
$23.5M
Impact of SAH on Parenchymal Arterioles and Neurovascular CouplingP01HL095488 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BONEV, ADRIAN · 2010 to 2014
$11.4M
REGULATION OF CEREBRAL ARTERY DILATIONR01HL044455 · NHLBI · UNIVERSITY OF VERMONT &ST AGRIC COLLEGE · PI NELSON, MARK T · 1991 to 2010
$3.9M
Ca2+ Sparks and Urinary Bladder Smooth Muscle ExcitabilityR37DK053832 · NIDDK · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI NELSON, MARK T · 2008 to 2017
$3.4M
Endothelial KCa channels, Ca2+ signaling & arteriolar function in the brainR01HL098243 · NHLBI · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI NELSON, MARK T · 2010 to 2010
$269k
NCRR NIH HHS P20 RR016435NCRR NIH HHS P20-RR-16435NHLBI NIH HHS P01 HL095488NHLBI NIH HHS P01-HL-095488NHLBI NIH HHS R01 HL044455NHLBI NIH HHS R01-HL-044455NHLBI NIH HHS R01 HL098243NHLBI NIH HHS R01-HL-098243NIDDK NIH HHS R37 DK053832NIDDK NIH HHS R37-DK-053832
6 · The paper itself

Abstract

For decades it has been known that external K(+) ions are rapid and potent vasodilators that increase CBF. Recent studies have implicated the local release of K(+) from astrocytic endfeet-which encase the entirety of the parenchymal vasculature-in the dynamic regulation of local CBF during NVC. It has been proposed that the activation of KIR channels in the vascular wall by external K(+) is a central component of these hyperemic responses; however, a number of significant gaps in our knowledge remain. Here, we explore the concept that vascular KIR channels are the major extracellular K(+) sensors in the control of CBF. We propose that K(+) is an ideal mediator of NVC, and discuss KIR channels as effectors that produce rapid hyperpolarization and robust vasodilation of cerebral arterioles. We provide evidence that KIR channels, of the KIR 2 subtype in particular, are present in both the endothelial and SM cells of parenchymal arterioles and propose that this dual positioning of KIR 2 channels increases the robustness of the vasodilation to external K(+), enables the endothelium to be actively engaged in NVC, and permits electrical signaling through the endothelial syncytium to promote upstream vasodilation to modulate CBF.

Indexed as

AnimalsBlood Flow VelocityEndothelium, VascularHumansMuscle, Smooth, VascularMyocytes, Smooth MuscleNeurovascular CouplingPotassium Channels, Inwardly RectifyingSignal TransductionVasodilationPotassium Channels, Inwardly Rectifyingastrocytic endfootcapillarycerebral blood flowendotheliumfunctional hyperemiainward rectifier potassium channelneurovascular couplingparenchymal arteriolesmooth muscle

Identifiers

PMID25641345
PMCPMC4404517
OpenAlexW2058760640

What OpenQuestion holds

Textmetadata
LicenceTDM
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.