The BK channel accessory β1 subunit determines alcohol-induced cerebrovascular constriction

Research output: Contribution to journalArticle

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Abstract

Ethanol-induced inhibition of myocyte large conductance, calcium- and voltage-gated potassium (BK) current causes cerebrovascular constriction, yet the molecular targets mediating EtOH action remain unknown. Using BK channel-forming (cbv1) subunits from cerebral artery myocytes, we demonstrate that EtOH potentiates and inhibits current at Cai 2 + lower and higher than ∼15 μM, respectively. By increasing cbv1's apparent Cai 2 +-sensitivity, accessory BK β1 subunits shift the activation-to-inhibition crossover of EtOH action to <3 μM Cai 2 +, with consequent inhibition of current under conditions found during myocyte contraction. Knocking-down KCNMB1 suppresses EtOH-reduction of arterial myocyte BK current and vessel diameter. Therefore, BK β1 is the molecular effector of alcohol-induced BK current inhibition and cerebrovascular constriction.

Original languageEnglish (US)
Pages (from-to)2779-2784
Number of pages6
JournalFEBS Letters
Volume583
Issue number17
DOIs
StatePublished - Sep 3 2009

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Large-Conductance Calcium-Activated Potassium Channels
Induced currents
Accessories
Constriction
Muscle Cells
Potassium
Ethanol
Chemical activation
Alcohols
Calcium
Electric potential
Cerebral Arteries

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Genetics
  • Molecular Biology
  • Structural Biology

Cite this

The BK channel accessory β1 subunit determines alcohol-induced cerebrovascular constriction. / Bukiya, Anna; Liu, Jianxi; Dopico, Alejandro.

In: FEBS Letters, Vol. 583, No. 17, 03.09.2009, p. 2779-2784.

Research output: Contribution to journalArticle

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