Chinese Journal of Tissue Engineering Research ›› 2021, Vol. 25 ›› Issue (17): 2630-2635.doi: 10.3969/j.issn.2095-4344.3190

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An 8-week aerobic exercise promotes the function of voltage-dependent potassium channel in mesenteric vascular smooth muscle from obese rats

Li Zihan, Yin Wen, Sun Wei, Zhu Kun, Shen Di, Liu Yujia   

  1. School of Physical Education, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, China
  • Received:2020-04-21 Revised:2020-04-24 Accepted:2020-05-27 Online:2021-06-18 Published:2021-01-07
  • Contact: Liu Yujia, MD, Lecturer, School of Physical Education, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, China
  • About author:Li Zihan, School of Physical Education, Jiangsu Normal University, Xuzhou 221116, Jiangsu Province, China
  • Supported by:
    the Natural Science Foundation of Jiangsu Province, No. BK20190999 (to LYJ); the Natural Science Foundation of Jiangsu Provincial Universities, No. 18KJB180003 (to LYJ); Jiangsu University Students' Innovation and Entrepreneurship General Project, No. 201910320142Y (to LZH)

Abstract: BACKGROUND: K+ channels in vascular smooth muscle cells play an important role in regulating vasodilation. Aerobic exercise that acts as a non-pharmacological way for weight loss can regulate vascular smooth muscle K+ channels. Whether aerobic exercise can improve the function and expression of obesity-induced vascular smooth muscle K+ channels has not been elucidated.   
OBJECTIVE: To investigate the effects of 8-week aerobic exercise on the K+ channel of mesenteric vascular smooth muscle in obese rats. 
METHODS: Sixty Sprague-Dawley rats (8 weeks old, male) were used in this study, 20 of which were fed with normal feed, and the other 40 were fed with high fat diet to induce obesity. Twenty obese rats were then obtained. Obese rats were randomized into an obese control group and an obese exercise group; normal rats were randomized into a normal control group and a normal exercise group, with 10 rats in each group. After all rats were adaptively trained for 1 week on the running platform, and those in the normal exercise and obese exercise group were then trained for another 8 weeks. The training plan was: 0°, 20 m/min, 60 min/d, 5 days a week. All rats were anesthetized and sacrificed 48 hours after the last exercise, and venous blood samples were extracted to measure blood sugar and blood lipid levels. Mesenteric artery was taken, a part of which was made into a vascular ring of about 4 mm that was connected to a tension transducer to test the vascular tension and reactivity of the vessel to the voltage-dependent potassium channel (Kv) specific blocker 4-aminopyridine and large-conductance calcium-activated potassium channel (BKCa) specific blocker charybdotoxin, and the other part of which was used to test the levels of Kv1.2, Kv1.5, BKCa α subunit and BKCa β1 subunit by western blot. 
RESULTS AND CONCLUSION:  (1) Body mass, heart weight, fasting blood glucose, triglyceride, low-density lipoprotein and total cholesterol in the obese exercise group were significantly lower than those in the obese control group (P < 0.01). (2) There was no significant difference in the reactivity of rat mesenteric arteries to KCl (P > 0.05). (3) The tension of the normal exercise group after 4-aminopyridine stimulation was significantly higher than that of the normal control group (P < 0.05); the tension of the obese exercise group after 4-aminopyridine stimulation was significantly higher than that of the obese control group (P < 0.05). (4) The reactivity of the normal exercise group to charybdotoxin was significantly higher than that of the normal control group (P < 0.05), but there was no significant difference between the obese control group and normal control group (P > 0.05). (5) The protein expression of Kv1.2 in the obese control group was significantly lower than that in the normal control group (P < 0.05), while the protein expression in the obese exercise group was significantly higher than that in the obese control group (P < 0.05). The protein expression of BKCa β1 in the normal exercise group was significantly higher than that in the normal control group (P < 0.05). There were no significant differences in the protein expressions of Kv1.5 and BKCa α among groups (P > 0.05). To conclude, obesity can decrease the function of Kv in mesenteric arteries, based on the mechanism underlying the reduction in the protein expression of Kv1.2, whereas the 8-week aerobic exercise reverses the reduction in Kv1.2 caused by obesity and promotes the function of Kv in mesenteric arteries. 

Key words: obesity, potassium channels, voltage-dependent, large-conductance calcium-activated potassium channel, aerobic exercise, rat, experiment 

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