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Rho‐kinase‐mediated suppression of KDR in cerebral arteries requires an intact actin cytoskeleton
Author(s) -
Luykenaar Kevin D,
Welsh Donald G
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.965.12
Subject(s) - actin cytoskeleton , cytochalasin d , cytoskeleton , microbiology and biotechnology , patch clamp , rho associated protein kinase , biology , cytochalasin , cerebral arteries , actin , chemistry , medicine , endocrinology , biophysics , electrophysiology , kinase , neuroscience , biochemistry , cell
This study examined the role of the actin cytoskeleton in Rho‐kinase‐mediated suppression of the delayed rectifier K + (K DR ) current in cerebral arteries. Myocytes from rat cerebral arteries were enzymatically isolated and whole cell K DR currents monitored using conventional patch clamp electrophysiology. At +40 mV, the K DR current averaged 19.8 ± 1.6 pA/pF (mean ± SE) and was potently inhibited by uridine triphosphate (UTP; 50 μM). Consistent with past observations, K DR suppression was blocked by the Rho‐kinase inhibitor Y‐27632 (30 μM). Likewise, disruption of the actin cytoskeleton using cytochalasin D (10 μM) or latrunculin A (10 nM) abolished the ability of UTP to suppress K DR . Interestingly, these agents inhibited the current when used at higher concentrations, further suggesting a mechanistic link between the actin cytoskeleton and channels underlying the K DR current. These preliminary findings suggest that an intact cytoskeletal framework is a requisite for Rho‐kinase‐mediated suppression of K DR current and the subsequent depolarization and constriction of cerebral arteries. Supported by CIHR and HSFC.