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Involvement of vascular Kv7 potassium channels in the pathogenesis of cerebral vasospasm
Author(s) -
Mani Bharath K,
Byron Kenneth L
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1140.7
Subject(s) - electrical impedance myography , depolarization , basilar artery , medicine , vasospasm , constriction , vasoconstriction , potassium channel , anesthesia , endocrinology , cardiology , subarachnoid hemorrhage , vasodilation
Cerebral vasospasm is a grave complication after subarachnoid hemorrhage characterized by persistent intense constriction of large conducting arteries in brain. Spastic contraction of the arterial myocytes is associated with membrane depolarization implicating calcium entry through voltage‐gated calcium channels. Endothelin, serotonin and vasopressin are spasmogens involved in the initiation and maintenance of vasospasm. We recently reported that Kv7 potassium channels are expressed in rat basilar artery myocytes and potassium conductance through the channels determine resting membrane potential and contractile status of basilar artery. Here we use patch‐clamp electrophysiology and pressure myography to test the involvement of Kv7 channels in the pathogenesis of cerebral vasospasm. Spasmogens suppressed Kv7 currents and produced membrane depolarization of basilar artery myocytes. The effects were reversed by Kv7 channel activator retigabine. Additivity experiments using pressure myography reveal the involvement of Kv7 channel suppression in the constriction produced by spasmogens. Activated PKC, a signal transduction intermediate of Gq‐coupled spasmogen receptor stimulation, suppressed Kv7 currents in myocytes and constricted basilar artery. These results indicate suppression of Kv7 currents as a mechanism for membrane depolarization and constriction of arteries by spasmogens resulting in vasospasm.