Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function

Gro Klitgaard Povlsen; Thomas A Longden; Adrian D. Bonev; David C. Hill-Eubanks; Mark T Nelson

doi:10.1177/0271678X16638350

Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function

Gro Klitgaard Povlsen, Thomas A Longden, Adrian D. Bonev, David C. Hill-Eubanks, Mark T Nelson

Division of Cardiovascular Sciences (L5)

Research output: Contribution to journal › Article › peer-review

Abstract

Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.

Original language	English
Pages (from-to)	1195-1201
Number of pages	7
Journal	Journal of Cerebral Blood Flow and Metabolism
Volume	36
Issue number	7
DOIs	https://doi.org/10.1177/0271678X16638350
Publication status	Published - Jul 2016

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Journal Article

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10.1177/0271678X16638350

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title = "Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function",

abstract = "Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.",

keywords = "Journal Article",

author = "Povlsen, {Gro Klitgaard} and Longden, {Thomas A} and Bonev, {Adrian D.} and Hill-Eubanks, {David C.} and Nelson, {Mark T}",

note = "{\textcopyright} The Author(s) 2016.",

year = "2016",

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doi = "10.1177/0271678X16638350",

language = "English",

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pages = "1195--1201",

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Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function. / Povlsen, Gro Klitgaard; Longden, Thomas A; Bonev, Adrian D. et al.
In: Journal of Cerebral Blood Flow and Metabolism, Vol. 36, No. 7, 07.2016, p. 1195-1201.

Research output: Contribution to journal › Article › peer-review

TY - JOUR

T1 - Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function

AU - Povlsen, Gro Klitgaard

AU - Longden, Thomas A

AU - Bonev, Adrian D.

AU - Hill-Eubanks, David C.

AU - Nelson, Mark T

PY - 2016/7

Y1 - 2016/7

N2 - Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.

AB - Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.

KW - Journal Article

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DO - 10.1177/0271678X16638350

M3 - Article

C2 - 27052838

SN - 1559-7016

VL - 36

SP - 1195

EP - 1201

JO - Journal of Cerebral Blood Flow and Metabolism

JF - Journal of Cerebral Blood Flow and Metabolism

IS - 7

ER -

Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function

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