Hypothermia Inhibits Endothelium-Independent Vascular Contractility via Rho-kinase Inhibition.
10.4062/biomolther.2016.233
- Author:
Yoon Hee CHUNG
1
;
Keon Woong OH
;
Sung Tae KIM
;
Eon Sub PARK
;
Hyun Dong JE
;
Hyuk Jun YOON
;
Uy Dong SOHN
;
Ji Hoon JEONG
;
Hyen Oh LA
Author Information
1. Department of Anatomy, College of Medicine, Chung-Ang University, Seoul 06974, Republic of Korea.
- Publication Type:Original Article
- Keywords:
ERK1/2;
fluoride;
hypothermia;
MYPT1;
phorbol ester;
Rho-kinase
- MeSH:
Animals;
Fluorides;
Humans;
Hypothermia*;
Isometric Contraction;
Male;
Muscle, Smooth, Vascular;
Nitric Oxide;
Phosphorylation;
Rats;
Relaxation;
rho-Associated Kinases*
- From:Biomolecules & Therapeutics
2018;26(2):139-145
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 A2-, 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 fluoride-induced 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.
