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Vascular plasticity in cerebrovascular disorders.

Edvinsson, Lars LU and Povlsen, Gro Klitgaard (2011) In Journal of Cerebral Blood Flow and Metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 31. p.1554-1571
Abstract
Cerebral ischemia remains a major cause of morbidity and mortality with little advancement in subacute treatment options. This review aims to cover and discuss novel insight obtained during the last decade into plastic changes in the vasoconstrictor receptor profiles of cerebral arteries and microvessels that takes place after different types of stroke. Receptors like the endothelin type B, angiotensin type 1, and 5-hydroxytryptamine type 1B/1D receptors are upregulated in the smooth muscle layer of cerebral arteries after different types of ischemic stroke as well as after subarachnoid hemorrhage, yielding rather dramatic changes in the contractility of the vessels. Some of the signal transduction processes mediating this receptor... (More)
Cerebral ischemia remains a major cause of morbidity and mortality with little advancement in subacute treatment options. This review aims to cover and discuss novel insight obtained during the last decade into plastic changes in the vasoconstrictor receptor profiles of cerebral arteries and microvessels that takes place after different types of stroke. Receptors like the endothelin type B, angiotensin type 1, and 5-hydroxytryptamine type 1B/1D receptors are upregulated in the smooth muscle layer of cerebral arteries after different types of ischemic stroke as well as after subarachnoid hemorrhage, yielding rather dramatic changes in the contractility of the vessels. Some of the signal transduction processes mediating this receptor upregulation have been elucidated. In particular the extracellular regulated kinase 1/2 pathway, which is activated early in the process, has proven to be a promising therapeutic target for prevention of vasoconstrictor receptor upregulation after stroke. Together, those findings provide new perspectives on the pathophysiology of ischemic stroke and point toward a novel way of reducing vasoconstriction, neuronal cell death, and thus neurologic deficits after stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 11 May 2011; doi:10.1038/jcbfm.2011.70. (Less)
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publication status
published
subject
in
Journal of Cerebral Blood Flow and Metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
volume
31
pages
1554 - 1571
publisher
Nature Publishing Group
external identifiers
  • wos:000292287800007
  • pmid:21559027
  • scopus:79959831866
ISSN
1559-7016
DOI
10.1038/jcbfm.2011.70
language
English
LU publication?
yes
id
8b4c75ac-9fc4-4f28-a138-6a21b1cc400c (old id 1972955)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/21559027?dopt=Abstract
date added to LUP
2011-06-07 15:20:31
date last changed
2017-08-13 04:38:48
@article{8b4c75ac-9fc4-4f28-a138-6a21b1cc400c,
  abstract     = {Cerebral ischemia remains a major cause of morbidity and mortality with little advancement in subacute treatment options. This review aims to cover and discuss novel insight obtained during the last decade into plastic changes in the vasoconstrictor receptor profiles of cerebral arteries and microvessels that takes place after different types of stroke. Receptors like the endothelin type B, angiotensin type 1, and 5-hydroxytryptamine type 1B/1D receptors are upregulated in the smooth muscle layer of cerebral arteries after different types of ischemic stroke as well as after subarachnoid hemorrhage, yielding rather dramatic changes in the contractility of the vessels. Some of the signal transduction processes mediating this receptor upregulation have been elucidated. In particular the extracellular regulated kinase 1/2 pathway, which is activated early in the process, has proven to be a promising therapeutic target for prevention of vasoconstrictor receptor upregulation after stroke. Together, those findings provide new perspectives on the pathophysiology of ischemic stroke and point toward a novel way of reducing vasoconstriction, neuronal cell death, and thus neurologic deficits after stroke.Journal of Cerebral Blood Flow & Metabolism advance online publication, 11 May 2011; doi:10.1038/jcbfm.2011.70.},
  author       = {Edvinsson, Lars and Povlsen, Gro Klitgaard},
  issn         = {1559-7016},
  language     = {eng},
  pages        = {1554--1571},
  publisher    = {Nature Publishing Group},
  series       = {Journal of Cerebral Blood Flow and Metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism},
  title        = {Vascular plasticity in cerebrovascular disorders.},
  url          = {http://dx.doi.org/10.1038/jcbfm.2011.70},
  volume       = {31},
  year         = {2011},
}