Voltage-gated K+ channel dysfunction in myocytes from a dog model of subarachnoid hemorrhage

Babak S. Jahromi, Yasuo Aihara, Jinglu Ai, Zhen Du Zhang, Elena Nikitina, Robert Loch MacDonald

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Delayed cerebral vasospasm after subarachnoid hemorrhage is primarily due to sustained contraction of arterial smooth muscle cells. Its pathogenesis remains unclear. The degree of arterial constriction is regulated by membrane potential that in turn is determined predominately by K+ conductance (GK). Here, we identified the main voltage-gated K+ (Kv) channels contributing to outward delayed rectifier currents in dog basilar artery smooth muscle as Kv2 class through a combination of electrophysiological and pharmacological methods. Kv2 current density was nearly halved in vasospastic myocytes after subarachnoid hemorrhage (SAH) in dogs, and Kv2.1 and Kv2.2 were downregulated in vasospastic myocytes when examined by quantitative mRNA, Western blotting, and immunohistochemistry. Vasospastic myocytes were depolarized and had a smaller contribution of GK toward maintenance of their membrane potential. Pharmacological block of Kv current in control myocytes mimicked the depolarization observed in vasospastic arteries. The degree of membrane depolarization was found to be compatible with the amount of vasoconstriction observed after SAH. We conclude that Kv2 dysfunction after SAH contributes to the pathogenesis of delayed cerebral vasospasm. This may confer a novel target for treatment of delayed cerebral vasospasm.

Original languageEnglish (US)
Pages (from-to)797-811
Number of pages15
JournalJournal of Cerebral Blood Flow and Metabolism
Issue number4
StatePublished - Apr 2008


  • Cerebral vasospasm
  • Delayed rectifier potassium channels
  • Subarachnoid hemorrhage

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine


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