Subarachnoid hemorrhage induces upregulation of vascular receptors and reduction in rCBF via an ERKI/2 mechanism

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Abstract

Previous studies have shown that endothelin type B (ETB) and 5-hydroxytryptamine type IB (5-HTIB) receptors are upregulated following subarachnoid hemorrhage (SAH). The purpose of the present study was to test whether extracellular signal-regulated kinase (ERKI/2) inhibition could alter the degree of SAH induced receptor upregulation in addition to prevent the cerebral blood flow (CBF) reduction. The ERKI/2 inhibitor SB386023-b was injected intra cisternally in conjunction with and after the induced SAH in rats. Two days after SAH cerebral arteries were harvested and the contractile response to endothelin-1 (ET-I) and 5-carboxamidotryptamine (5-CT) were investigated with a myograph. The contractile responses to ET-I and 5-CT were increased after SAH compared to sham. Administration of SB-386023-b prevented the upregulated contraction elicited by application of ET-I and 5-CT in cerebral arteries. Regional CBF evaluated by an autoradiographic technique, revealed a reduced CBF by 50% after SAH this was prevented by treatment with SB-386023-b. The results indicate that an ERKI/2 mechanism is involved in cerebral vasospasm and ischemia associated with SAH.
Original languageEnglish
Title of host publicationCerebral Vasospasm: New Strategies in Research and Treatment
PublisherSpringer
Pages65-67
Volume104
ISBN (Print)978-3-211-75717-8
DOIs
Publication statusPublished - 2008
Event9th International Conference on Cerebral Vasospasm - Istanbul, Turkey
Duration: 2006 Jun 272006 Jun 30

Publication series

Name
Volume104
ISSN (Print)0065-1419

Conference

Conference9th International Conference on Cerebral Vasospasm
Country/TerritoryTurkey
CityIstanbul
Period2006/06/272006/06/30

Subject classification (UKÄ)

  • Other Clinical Medicine

Free keywords

  • signal-regulated kinase (ERKI/2)
  • extracellular
  • cerebral blood flow (CBF)
  • cerebral ischemia
  • subarachnoid hemorrhage (SAH)

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