衰老大鼠动脉超微结构及平滑肌钾通道反应性变化  

Changes of arterial ultrastructure and reaction of potassium channels in smooth muscle in aged rats

作　　者：孙华灵[1] 石丽君[1] 李丽[1] 刘晓东[1] 

机构地区：[1]北京体育大学运动生理教研室,北京市100084

出　　处：《中国组织工程研究》2013年第41期7228-7234,共7页Chinese Journal of Tissue Engineering Research

基　　金：国家自然科学基金(31071033);教育部新世纪优秀人才培养资助(NCET-11-0850);北京市自然科学基金(5132017)~~

摘　　要：背景:K^+通道是调节血管平滑肌的收缩性与舒张性的主要离子通道,与血管张力息息相关,但对K+通道在机体衰老过程中的作用鲜有报道。目的:观察衰老对大鼠动脉超微结构和平滑肌钾通道反应性的影响及可能的作用机制。方法:健康雄性Wistar大鼠16只,19月龄设为老年组(n=8),2月龄设为青年组(n=8)。两组各随机抽取6只大鼠进行胸主动脉血管环张力测定,分别给予钙激活钾通道特异性阻断剂TEA、电压依赖性钾通道特异性阻断剂4-AP、ATP敏感性钾通道特异性阻断剂glibenclamide、内向整流钾通道的特异性阻断剂BaCl_2等药物刺激,观察各阻断剂引起的动脉反应性变化。余下每组2只,取胸主动脉以透射电镜观察动脉超微结构的变化。结果与结论:与青年组大鼠比较,老年组胸主动脉内皮细胞和平滑肌细胞等结构发生衰老性变化;KCl诱发大鼠胸主动脉达到最大收缩张力后恢复基础张力所需时间,老年组明显长于青年组;4种阻断剂均诱发血管张力增加,且TEA和4-AP诱发的胸主动脉收缩反应,老年组显著低于青年组;glibenclamide和BaCl_2诱发的血管收缩两组间无显著性差异。说明衰老可引起大鼠动脉超微结构发生改变,血管舒张能力下降,其中平滑肌钾通道尤其是钙激活钾通道和电压依赖性钾通道功能下降可能是其重要机制之一。BACKGROUND： Potassium channel is the main ion channel to regulate vascular smooth muscle contraction and relaxation, and closely related with vascular tone. However, the reports about the mechanism of potassium channels in the body＇s aging process are rare. OBJECTIVE： To investigate the effects of aging on the arterial ultrastructure and smooth muscle potassium channel reaction, and then to explore the possible mechanisms. METHODS： Sixteen healthy male Wistar rats were collected, 19-month-old rats were assigned to the old group （n=8）, 2-month-old rats were used as young group （n=8）. The thoracic arteries were isolated and cut into rings to conduct contractility measurement in six rats of each group. The thoracic arteries were stimulated with specific calcium-activated potassium channel blocker tetraethylammonium, specific voltage-dependent potassium channel blocker 4-aminopyridine, specific ATP-sensitive potassium channel blocker glibenclamide, and specific inward rectifier potassium channel blocker BaCI2, and then the arterial contractile response to the blockers were observed. The thoracic arteries of the remaining two rats in each group were taken to observe the arterial ultrastructure changes under electron microscope. RESULTS AND CONCLUSION： Compared with the young group, the ultrastructures of the thoracic aortic endothelial cells and smooth muscle cells were changed in the old group; KCI induced the maximum thoracicaortic contractile tension, and then recovered to the baseline tension, and the recovery time in the old group was significantly longer than that in the young group; all the four kinds of blockers could increase vascular tone, and the tetraethylammonium and 4-aminopyridine induced thoracic aortic contractile response in the old group was significantly lower than that in the young group; there was no significant difference in vasoconstriction induced by glibenclamide and BaCl2. Aging can induce arterial ultrastructure changes and declination of vasodilatation capacity, which may

关 键 词：组织构建 血管组织构建 衰老 胸主动脉 动脉 超微结构 钾通道 阻断剂 国家自然科学基金 

分 类 号：R318[医药卫生—生物医学工程]