Vascular Inward Rectifier K+ Channels as External K+ Sensors in the Control of Cerebral Blood Flow

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 b...

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Bibliographic Details
Published in:Microcirculation (New York, N.Y. 1994) Vol. 22; no. 3; pp. 183 - 196
Main Authors: Longden, Thomas A., Nelson, Mark T.
Format: Journal Article
Language:English
Published: United States Blackwell Publishing Ltd 01.04.2015
Wiley Subscription Services, Inc
Subjects:
Animals
astrocytic endfoot
Blood
Blood Flow Velocity - physiology
capillary
cerebral blood flow
endothelium
Endothelium, Vascular - metabolism
functional hyperemia
Humans
inward rectifier potassium channel
Muscle, Smooth, Vascular - metabolism
Myocytes, Smooth Muscle - metabolism
neurovascular coupling
Neurovascular Coupling - physiology
parenchymal arteriole
Potassium Channels, Inwardly Rectifying - genetics
Potassium Channels, Inwardly Rectifying - metabolism
Signal Transduction - physiology
smooth muscle
Vasodilation - physiology
endothelium
capillary
neurovascular coupling
smooth muscle
cerebral blood flow
functional hyperemia
parenchymal arteriole
astrocytic endfoot
inward rectifier potassium channel
ISSN:1073-9688, 1549-8719, 1549-8719
Online Access:Get full text
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Summary: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 KIR2 subtype in particular, are present in both the endothelial and SM cells of parenchymal arterioles and propose that this dual positioning of KIR2 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.
Bibliography:Totman Medical Research Trust
Fondation Leducq
ark:/67375/WNG-F1HNVST0-7
American Heart Association - No. 12POST12090001; No. 14POST20480144
ArticleID:MICC12190
istex:83C27778C1D89ADF6CFB4FF2FF010D0B929B1859
National Institutes of Health - No. P20-RR-16435; No. P01-HL-095488; No. R01-HL-044455; No. R01-HL-098243; No. R37-DK-053832
ObjectType-Article-1
SourceType-Scholarly Journals-1
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ISSN:1073-9688
1549-8719
1549-8719
DOI:10.1111/micc.12190