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Decreased frequency of transient outward BK currents in cerebral myocytes following subarachnoid hemorrhage
Author(s) -
Koide Masayo,
Krishnamoorthy Gayathri,
O’Connor Kevin P,
Nelson Mark T,
Wellman George C
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.22.1_supplement.965.18
Subject(s) - subarachnoid hemorrhage , bk channel , cerebral vasospasm , vasospasm , potassium channel , medicine , patch clamp , depolarization , vasoconstriction , cerebral arteries , myocyte , cardiology , anesthesia , chemistry , endocrinology , electrophysiology
Cerebral vasospasm is a prolonged vasoconstriction causing substantial morbidity and mortality in patients following aneurysmal and subarachnoid hemorrhage (SAH). The mechanisms underlying this pathology remain unclear, but may involve decreased K + channel activity in cerebral artery myocytes. Ca 2+ sparks are localized intracellular Ca 2+ release events leading to the transient activation of large conductance Ca 2+ ‐activated K + (BK) channels. Here, we evaluated transient BK currents in freshly isolated cerebral artery myocytes obtained from a rabbit model of SAH. Transient whole cell BK currents and single channel BK properties were examined using the perforated whole cell and single channel patch‐clamp technique, respectively. We also examined BK channel α and β1 subunit expression using RT‐PCR. Transient BK current frequency was decreased in cerebral artery myocytes from SAH rabbits, however BK channel properties (voltage‐ and Ca 2+ ‐dependence) and expression were unchanged. These data suggest decreased Ca 2+ spark frequency or an uncoupling between Ca 2+ spark and BK channel activation may underlie the observed decrease in transient BK frequency. A reduction in BK channel activity in cerebral artery myocytes may contribute to cerebral vasospasm following SAH. This work was supported by the Totman Medical Research Trust, the Peter Martin Brain Aneurysm Endowment, the AHA and the NIH.