Biomol Ther.  2018 Mar;26(2):139-145. 10.4062/biomolther.2016.233.

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

• Chung YH
• Oh KW
• Kim ST
• Park ES
• Je HD
• Yoon HJ
• Sohn UD
• Jeong JH
• La HO

• KMID: 2429053
• DOI: http://doi.org/10.4062/biomolther.2016.233

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.

Keyword

ERK1/2; fluoride; hypothermia; MYPT1; phorbol ester; Rho-kinase

MeSH Terms

Animals
Fluorides
Humans
Hypothermia*
Isometric Contraction
Male
Muscle, Smooth, Vascular
Nitric Oxide
Phosphorylation
Rats
Relaxation
rho-Associated Kinases*
Fluorides
Nitric Oxide
rho-Associated Kinases