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Modulation by superoxide of delayed rectifier K+ channel current in rat cerebral arterial muscle cells.
Author(s) -
Gebremedhin Debebe,
Harder David R.
Publication year - 2008
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.22.2_supplement.144
Subject(s) - superoxide , chemistry , patch clamp , tiron , potassium channel , biophysics , myocyte , medicine , biochemistry , biology , enzyme , receptor
The effect of superoxide released from potassium peroxide (KO 2 ) was evaluated on the activities of delayed rectifier unitary and macroscopic K + current (I Kdr ) in rat cerebral arterial muscle cells recorded using the patch clamp technique. External application of superoxide (at 10 and 30 μmol/L) caused the opening frequency and NPo of a 48 ± 4 pS single‐channel delayed rectifier K + channel current to increase during recording from a cell‐attached patch. Excision of an inside‐out patch elicited a slight increase in the NPo of the single‐channel but treatment of the inside‐out patch with 30 μM superoxide had no effect on both the opening frequency and NPo of the 48 pS I Kdr channel current. Similar external application of superoxide significantly increased the magnitude of whole‐cell or macroscopic delayed rectifier K + channel current without shifting the voltage‐dependency of I Kdr channel current activation. Superoxide at the concentrations used failed to increase either the NPo of the 48 pS single‐channel I Kdr current or the magnitude of the whole‐cell macroscopic I Kdr channel current following treatment of the cells with 4‐aminopyridine (1 mM) or with the superoxide scavenger tiron (1 μM). This findings suggest that modulation by superoxide of the delayed rectifier K + channel current in cerebral arterial muscle cells is indirect, and could be one of the mechanisms by which superoxide modulate the excitability of the cerebral arterial muscle cells.