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Cerebral vasoconstriction after subarachnoid hemorrhage - Role of changes in vascular receptor phenotype

Hansen-Schwartz, Jacob LU ; Ansar, Saema and Edvinsson, Lars LU (2008) In Frontiers in Bioscience 13. p.2160-2164
Abstract
The pathological constriction of cerebral arteries known as cerebral vasospasm (CVS) is with a delay of 4 to 10 days linked to subarachnoid hemorrhage. Several agents have been suggested as being responsible; amongst these perhaps 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) are the most prominent given their ability to elicit powerful constriction of cerebral arteries. Investigating both 5-HT and ET receptors we have observed that there are distinct changes in receptor phenotype after experimental SAH, namely upregulation of the ETB and 5-HT1B receptors, and that this upregulation is linked to a higher sensitivity to the endogenous agonists. It has also been shown that reduction in regional cerebral blood flow (CBF) is associated... (More)
The pathological constriction of cerebral arteries known as cerebral vasospasm (CVS) is with a delay of 4 to 10 days linked to subarachnoid hemorrhage. Several agents have been suggested as being responsible; amongst these perhaps 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) are the most prominent given their ability to elicit powerful constriction of cerebral arteries. Investigating both 5-HT and ET receptors we have observed that there are distinct changes in receptor phenotype after experimental SAH, namely upregulation of the ETB and 5-HT1B receptors, and that this upregulation is linked to a higher sensitivity to the endogenous agonists. It has also been shown that reduction in regional cerebral blood flow (CBF) is associated with receptor upregulation and interventional animal experiments have shown a benefit from inhibiting the PKC and MAP kinase pathways on receptor upregulation, CBF and neurological outcome. (Less)
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type
Contribution to journal
publication status
published
subject
keywords
review, subarachnoid haemorrhage, reverse transcriptase polymerase chain reaction, pharmacology, in vitro, organ culture, endothelin receptors, 5-HT receptors
in
Frontiers in Bioscience
volume
13
pages
2160 - 2164
publisher
Frontiers in Bioscience
external identifiers
  • wos:000255775700175
  • scopus:38449099843
ISSN
1093-9946
DOI
10.2741/2831
language
English
LU publication?
yes
id
68de00dd-6a5d-49dd-85f1-ba9554cd6848 (old id 1191405)
date added to LUP
2016-04-01 12:28:52
date last changed
2024-01-08 21:57:46
@article{68de00dd-6a5d-49dd-85f1-ba9554cd6848,
  abstract     = {{The pathological constriction of cerebral arteries known as cerebral vasospasm (CVS) is with a delay of 4 to 10 days linked to subarachnoid hemorrhage. Several agents have been suggested as being responsible; amongst these perhaps 5-hydroxytryptamine (5-HT) and endothelin-1 (ET-1) are the most prominent given their ability to elicit powerful constriction of cerebral arteries. Investigating both 5-HT and ET receptors we have observed that there are distinct changes in receptor phenotype after experimental SAH, namely upregulation of the ETB and 5-HT1B receptors, and that this upregulation is linked to a higher sensitivity to the endogenous agonists. It has also been shown that reduction in regional cerebral blood flow (CBF) is associated with receptor upregulation and interventional animal experiments have shown a benefit from inhibiting the PKC and MAP kinase pathways on receptor upregulation, CBF and neurological outcome.}},
  author       = {{Hansen-Schwartz, Jacob and Ansar, Saema and Edvinsson, Lars}},
  issn         = {{1093-9946}},
  keywords     = {{review; subarachnoid haemorrhage; reverse transcriptase polymerase chain reaction; pharmacology; in vitro; organ culture; endothelin receptors; 5-HT receptors}},
  language     = {{eng}},
  pages        = {{2160--2164}},
  publisher    = {{Frontiers in Bioscience}},
  series       = {{Frontiers in Bioscience}},
  title        = {{Cerebral vasoconstriction after subarachnoid hemorrhage - Role of changes in vascular receptor phenotype}},
  url          = {{http://dx.doi.org/10.2741/2831}},
  doi          = {{10.2741/2831}},
  volume       = {{13}},
  year         = {{2008}},
}