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Hypothermia Inhibits Endothelium-Independent Vascular Contractility via Rho-kinase Inhibition

The present study was undertaken to investigate the influence of hypothermia on endothelium-independent vascular smooth muscle contractility and to determine the mechanism underlying the relaxation. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined w...

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Bibliographic Details
Published in:Biomolecules & therapeutics 2018, 26(2), , pp.139-145
Main Authors: Chung, Yoon Hee, Oh, Keon Woong, Kim, Sung Tae, Park, Eon Sub, Je, Hyun Dong, Yoon, Hyuk-Jun, Sohn, Uy Dong, Jeong, Ji Hoon, La, Hyen-Oh
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Language:English
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Summary:The present study was undertaken to investigate the influence of hypothermia on endothelium-independent vascular smooth muscle contractility and to determine the mechanism underlying the relaxation. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Hypothermia significantly inhibited fluoride-, thromboxane A 2- , phenylephrine-, and phorbol ester-induced vascular contractions regardless of endothelial nitric oxide synthesis, suggesting that another pathway had a direct effect on vascular smooth muscle. Hypothermia significantly inhibited the fluorideinduced increase in pMYPT1 level and phorbol ester-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxing effect of moderate hypothermia on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activities.
ISSN:1976-9148
2005-4483
1976-9148
2005-4483
DOI:10.4062/biomolther.2016.233