• Fang Yuan, Hong-Wei Li, Shi-Jun Song, Xu Teng, Hui-Jie Ma, Zan Guo, Yi Zhang, and Zhao-Nian Zhou.
• Department of Physiology, Hebei Medical University, Shijiazhuang 050017, China; Department of Physiology, Xingtai Medical College, Xingtai 054000, China; Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China; Hebei Key Laboratory of Laboratory Animal Science, Shijiazhuang 050017, China; Hebei Key Laboratory of Medical Biotechnology, Shijiazhuang 050017, China. E-mail: zhyhenry@hotmail.com.
• Sheng Li Xue Bao. 2013 Jun 25; 65 (3): 269-75.

AbstractThe present study was designed to investigate the role of opioid receptors in the vasorelaxation effect of chronic intermittent hypobaric hypoxia (CIHH) in thoracic aorta rings and the underlying mechanism in rats. Adult male Sprague-Dawley (SD) rats were randomly divided into 2 groups: CIHH treatment group and control group. The rats in CIHH group were exposed to hypoxia in a hypobaric chamber (simulated 5 000 m altitude) for 28 days, 6 h per day. The rats in control group were kept in the same environment as CIHH rats except no hypoxia exposure. The relaxation of thoracic aorta rings was recorded by organ bath perfusion technique, and expression of opioid receptors was measured by Western blot. Results are shown as follows. (1) The acetylcholine (ACh)-induced endothelium-dependent relaxation of thoracic aorta in CIHH rats was increased obviously in a concentration-dependent manner compared with that in control rats (P < 0.05). (2) This enhancement of ACh-induced relaxation in CIHH rats was abolished by naloxone, a non-specific opioid receptor blocker (P < 0.05). (3) The expressions of δ, μ and κ opioid receptors in thoracic aorta of CIHH rats were up-regulated compared with those in control rats (P < 0.05). (4) The enhancement of CIHH on relaxation of thoracic aorta was reversed by glibenclamide, an ATP-sensitive potassium channel (KATP) blocker (P < 0.05). The results suggest that opioid receptors are involved in CIHH-enhanced ACh-induced vasorelaxation of thoracic aorta through KATP channel pathways.

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