摘要
目的探讨大负荷运动通过一氧化氮(NO)信号通路降低高血压的可能机制。方法利用大鼠高血压模型进行大负荷运动。采用酶化学方法检测大白鼠血液中一氧化氮合酶(NOS)活性及NO水平变化,反转录多聚酶链反应检测大白鼠大动脉组织中NO和NOS的mRNA水平,免疫印迹实验检测大白鼠大动脉组织中VEGF蛋白水平的变化及动脉血管组织Akt,PI3K水平。结果运动组血液中NOS活性及NO的蛋白表达水平显著高于静息组(P<0.05);运动组大动脉组织中NOS活性、NO的mRNA水平、激活型Akt、PI3K水平显著高于静息组(P<0.05),而总Akt、PI3K蛋白水平没有明显增高(P>0.05)。结论大负荷运动可增强组织中的Akt、PI3K活性,从而调节血液中NOS活性,调节血液中NO水平,并最终降低高血压。
Objective To study the mechanism of overtraining effect on hypertension by nitric oxide signaling pathway. Methods Hypertension model mouse was used to detect the changes of blood pressure upon overtraining. Enzymatic activity assays were used for detecting the level of NO and NOS activity. The expressions of VEGF, p-Akt and p-PI3K were detected by Western blotting. Results Blood pressure monitor assay showed that aerobic exercise have the potential role in decreasing the blood pressure. The level of blood NO increased significantly（P 〈 0.05 ） in the aerobic exercise group, and the activity of NOS in the aerobic exercise group increased evidently（ P 〈 0.05 ） compared to the resting group. The level of VEGF-C, p-Akt and p-PI3K increased markedly（P 〈 0.05 ） in aerobic exercise group compared to the resting group, but the total Akt and PI3K protein levels were not enhanced （P 〉 0.05） compared with the resting group. Conclusion Overtraining can enhance the organization Akt, PI3K activity, thereby regulating the activity of NOS in the blood, regulate the blood levels of NO, and ultimately reduce high blood pressure.
出处
《健康研究》
CAS
2013年第1期25-28,共4页
Health Research
关键词
一氧化氮信号通路
运动
高血压
nitric oxide signaling pathway
exercise
hypertension
