Acetylcholine-induced AMP-activated protein kinase activation attenuates vasoconstriction through an LKB1-dependent mechanism in rat aorta

Title
Acetylcholine-induced AMP-activated protein kinase activation attenuates vasoconstriction through an LKB1-dependent mechanism in rat aorta
Author(s)
최형철이경영
Keywords
SMOOTH-MUSCLE-CELLS; LIGHT-CHAIN KINASE; SPONTANEOUSLY HYPERTENSIVE-RATS; ENDOTHELIAL-CELLS; CONTRACTION; METFORMIN; VASODILATATION; VASORELAXATION; OXIDATION; MICE
Issue Date
201310
Publisher
ELSEVIER SCIENCE INC
Citation
VASCULAR PHARMACOLOGY, v.59, no.3-4, pp.96 - 102
Abstract
Numerous studies of acetylcholine (ACh)-induced endothelium-dependent relaxation in arteries have been reported since the original description by Furchgott and Zawadzki (1980). ACh also produces endothelium-independent relaxation. However, it is still unknown whether ACh-induced AMP-activated protein kinase (AMPK) activation can attenuate vasoconstriction in endothelium-denuded rat aorta. Here, we investigated whether ACh may exert a regulatory effect for vascular tone via AMPK activation and its underlying mechanism in vascular smooth muscle cells (VSMCs). Western blotting showed that ACh dose- and time-dependently increased LKB1 and AMPK phosphorylation in VSMCs. The ACh-induced activation of AMPK required muscarinic receptors in VSMCs. LKB1 and AMPK activation by ACh inhibited myosin light-chain kinase (MLCK) and phosphorylated myosin light chain (p-MLC) expression in VSMCs. In addition, a tension study showed the inhibitory effect of ACh-induced AMPK activation on phenylephrine-mediated contraction in endothelium-denuded rat aorta. These data suggest that the ACh-induced activation of AMPK may attenuate vasoconstriction via LKB1-AMPK-dependent mechanism in endothelium-denuded rat aorta. (C) 2013 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/28804http://dx.doi.org/10.1016/j.vph.2013.07.007
ISSN
1537-1891
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의과대학 > 약리학교실 > Articles
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