Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats

Research output: Contribution to journal › Journal article › Research › peer-review

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Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats. / Johansson, S E; Andersen, X E D R; Hansen, R H; Povlsen, G K; Edvinsson, L.

In: Acta Physiologica (Print), Vol. 214, No. 3, 07.2015, p. 376-89.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Johansson, SE, Andersen, XEDR, Hansen, RH, Povlsen, GK & Edvinsson, L 2015, 'Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats', Acta Physiologica (Print), vol. 214, no. 3, pp. 376-89. https://doi.org/10.1111/apha.12519

APA

Johansson, S. E., Andersen, X. E. D. R., Hansen, R. H., Povlsen, G. K., & Edvinsson, L. (2015). Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats. Acta Physiologica (Print), 214(3), 376-89. https://doi.org/10.1111/apha.12519

Vancouver

Johansson SE, Andersen XEDR, Hansen RH, Povlsen GK, Edvinsson L. Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats. Acta Physiologica (Print). 2015 Jul;214(3):376-89. https://doi.org/10.1111/apha.12519

Author

Johansson, S E ; Andersen, X E D R ; Hansen, R H ; Povlsen, G K ; Edvinsson, L. / Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats. In: Acta Physiologica (Print). 2015 ; Vol. 214, No. 3. pp. 376-89.

Bibtex

@article{a43bdd55d3274f128c7f5f97fadc3889,
title = "Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats",
abstract = "AIM: In this study, we aimed to investigate whether changes in cerebrovascular voltage-dependent calcium channels and non-selective cation channels contribute to the enhanced endothelin-1-mediated vasoconstriction in the delayed hypoperfusion phase after experimental transient forebrain ischaemia.METHODS: Experimental forebrain ischaemia was induced in Wistar male rats by a two-vessel occlusion model, and the cerebral blood flow was measured by magnetic resonance imaging two days after reperfusion. In vitro vasoreactivity studies, immunofluorescence and quantitative PCR were performed on cerebral arteries from ischaemic or sham-operated rats to evaluate changes in vascular voltage-dependent calcium channels, transient receptor potential canonical channels as well as endothelin-1 receptor function and expression.RESULTS: The expression of transient receptor potential canonical channels 1 and 6 in the vascular smooth muscle cells was enhanced and correlated with decreased cerebral blood flow two days after forebrain ischaemia. Furthermore, under conditions when voltage-dependent calcium channels were inhibited, endothelin-1-induced cerebrovascular contraction was enhanced and this enhancement was presumably mediated by Ca(2+) influx via upregulated transient receptor potential canonical channels 1 and 6.CONCLUSIONS: Our data demonstrates that endothelin-1-mediated influx of extracellular Ca(2+) activates transient receptor potential canonical channels 1 and 6 in cerebral vascular smooth muscle cells. This seems to have an important role in the enhanced cerebral vasoconstriction in the delayed post-ischaemic hypoperfusion phase after experimental forebrain ischaemia.",
keywords = "Animals, Blood Flow Velocity, Brain Ischemia, Calcium Signaling, Cerebrovascular Circulation, Endothelin-1, Male, Prosencephalon, Rats, Rats, Wistar, TRPC Cation Channels",
author = "Johansson, {S E} and Andersen, {X E D R} and Hansen, {R H} and Povlsen, {G K} and L Edvinsson",
note = "{\textcopyright} 2015 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.",
year = "2015",
month = jul,
doi = "10.1111/apha.12519",
language = "English",
volume = "214",
pages = "376--89",
journal = "Acta Physiologica",
issn = "1748-1708",
publisher = "Wiley-Blackwell",
number = "3",

}

RIS

TY - JOUR

T1 - Cerebrovascular endothelin-1 hyper-reactivity is associated with transient receptor potential canonical channels 1 and 6 activation and delayed cerebral hypoperfusion after forebrain ischaemia in rats

AU - Johansson, S E

AU - Andersen, X E D R

AU - Hansen, R H

AU - Povlsen, G K

AU - Edvinsson, L

N1 - © 2015 Scandinavian Physiological Society. Published by John Wiley & Sons Ltd.

PY - 2015/7

Y1 - 2015/7

N2 - AIM: In this study, we aimed to investigate whether changes in cerebrovascular voltage-dependent calcium channels and non-selective cation channels contribute to the enhanced endothelin-1-mediated vasoconstriction in the delayed hypoperfusion phase after experimental transient forebrain ischaemia.METHODS: Experimental forebrain ischaemia was induced in Wistar male rats by a two-vessel occlusion model, and the cerebral blood flow was measured by magnetic resonance imaging two days after reperfusion. In vitro vasoreactivity studies, immunofluorescence and quantitative PCR were performed on cerebral arteries from ischaemic or sham-operated rats to evaluate changes in vascular voltage-dependent calcium channels, transient receptor potential canonical channels as well as endothelin-1 receptor function and expression.RESULTS: The expression of transient receptor potential canonical channels 1 and 6 in the vascular smooth muscle cells was enhanced and correlated with decreased cerebral blood flow two days after forebrain ischaemia. Furthermore, under conditions when voltage-dependent calcium channels were inhibited, endothelin-1-induced cerebrovascular contraction was enhanced and this enhancement was presumably mediated by Ca(2+) influx via upregulated transient receptor potential canonical channels 1 and 6.CONCLUSIONS: Our data demonstrates that endothelin-1-mediated influx of extracellular Ca(2+) activates transient receptor potential canonical channels 1 and 6 in cerebral vascular smooth muscle cells. This seems to have an important role in the enhanced cerebral vasoconstriction in the delayed post-ischaemic hypoperfusion phase after experimental forebrain ischaemia.

AB - AIM: In this study, we aimed to investigate whether changes in cerebrovascular voltage-dependent calcium channels and non-selective cation channels contribute to the enhanced endothelin-1-mediated vasoconstriction in the delayed hypoperfusion phase after experimental transient forebrain ischaemia.METHODS: Experimental forebrain ischaemia was induced in Wistar male rats by a two-vessel occlusion model, and the cerebral blood flow was measured by magnetic resonance imaging two days after reperfusion. In vitro vasoreactivity studies, immunofluorescence and quantitative PCR were performed on cerebral arteries from ischaemic or sham-operated rats to evaluate changes in vascular voltage-dependent calcium channels, transient receptor potential canonical channels as well as endothelin-1 receptor function and expression.RESULTS: The expression of transient receptor potential canonical channels 1 and 6 in the vascular smooth muscle cells was enhanced and correlated with decreased cerebral blood flow two days after forebrain ischaemia. Furthermore, under conditions when voltage-dependent calcium channels were inhibited, endothelin-1-induced cerebrovascular contraction was enhanced and this enhancement was presumably mediated by Ca(2+) influx via upregulated transient receptor potential canonical channels 1 and 6.CONCLUSIONS: Our data demonstrates that endothelin-1-mediated influx of extracellular Ca(2+) activates transient receptor potential canonical channels 1 and 6 in cerebral vascular smooth muscle cells. This seems to have an important role in the enhanced cerebral vasoconstriction in the delayed post-ischaemic hypoperfusion phase after experimental forebrain ischaemia.

KW - Animals

KW - Blood Flow Velocity

KW - Brain Ischemia

KW - Calcium Signaling

KW - Cerebrovascular Circulation

KW - Endothelin-1

KW - Male

KW - Prosencephalon

KW - Rats

KW - Rats, Wistar

KW - TRPC Cation Channels

U2 - 10.1111/apha.12519

DO - 10.1111/apha.12519

M3 - Journal article

C2 - 25939574

VL - 214

SP - 376

EP - 389

JO - Acta Physiologica

JF - Acta Physiologica

SN - 1748-1708

IS - 3

ER -

ID: 160099701