CaMKII inhibition with KN93 attenuates endothelin and serotonin receptor-mediated vasoconstriction and prevents subarachnoid hemorrhage-induced deficits in sensorimotor function.

Lars Edvinsson, Gro Klitgaard Povlsen, Hilda Ahnstedt, Roya Waldsee

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskriftPeer review

10 Citeringar (SciVal)
145 Nedladdningar (Pure)

Sammanfattning

It has been suggested that transcriptional upregulation of cerebral artery contractile endothelin (ETB) and 5-hydroxytryptamine (5-HT1B) receptors play an important role in the development of late cerebral ischemia and increased vasoconstriction after subarachnoid hemorrhage (SAH). We tested the hypothesis that inhibition of calcium calmodulin-dependent protein kinase II (CaMKII) may reduce cerebral vasoconstriction mediated by endothelin and serotonin receptors and improve neurological outcome after experimental SAH.
Originalspråkengelska
Artikelnummer207
TidskriftJournal of Neuroinflammation
Volym11
DOI
StatusPublished - 2014

Ämnesklassifikation (UKÄ)

  • Neurologi

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