Abstract
Objective: Recent studies showed that the cytoskeleton is the primary target of reactive oxygen species (ROS). This study examines the role of cytoskeleton network in regulation of vascular smooth muscle cell contractions by ROS. Design and Methods: Contractile responses of rat aorta strips triggered by depolarization and activation of α1-adrenergic receptors with high K+-medium and phenylephrine, respectively, were measured as increments of isometric tension. Cytoskeleton elements were modified with colchicines (10 μM), cytochalasin D (0,5 μM) and nocodazole (10 μM). Production of ROS was evoked by hydrogen peroxide (500 μM). Results: Hydrogen peroxide increased contractions triggered by high-K+ -medium by 25,2 ± 2,9% (p < 0,05) and reduced the amplitude of phenylephrine-induced contractile responses by 51,7 ± 2,9% (p < 0,05). Colchicine and cytochalasin D, but not nocodazole increased the relaxing effect of hydrogen peroxide in the reduction of phenylephrine-induced contractions by 83,5 ± 4,1% (p < 0,05) and 89,4 ± 2,9% (p < 0,05), respectively, but did not affect modulation by ROS of contractions triggered by depolarization. Conclusion: Our data demonstrate the involvement of cytoskeleton-mediated signaling in regulation by ROS of vascular smooth muscle cell contractions caused by activation of - α1-adrenergic receptors.
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