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
Department of Anatomy, College of Medicine, Chung-Ang University, Seoul 06974, Republic of Korea.
Department of Pathology, College of Medicine, Chung-Ang University, Seoul 06974, Republic of Korea.
Biomol Ther (Seoul). 2018 Mar 1;26(2):139-145. doi: 10.4062/biomolther.2016.233.
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-, 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.
本研究旨在探讨低温对内皮依赖性血管平滑肌收缩性的影响，并确定其舒张的潜在机制。使用雄性大鼠的去内皮主动脉环，记录等长收缩，并结合分子实验。无论内皮一氧化氮合成情况如何，低温均显著抑制氟化物、血栓素A、去氧肾上腺素和佛波酯诱导的血管收缩，提示另一条途径对血管平滑肌有直接作用。低温显著抑制氟化物诱导的pMYPT1水平升高和佛波酯诱导的pERK1/2水平升高，提示抑制Rho激酶和MEK活性以及随后的MYPT1和ERK1/2磷酸化。这些结果表明，中度低温对激动剂诱导的血管收缩的舒张作用，无论内皮功能如何，都涉及抑制Rho激酶和MEK活性。
