应激大鼠下丘脑血管紧张素原mRNA的表达

Expression of angiotensinogen mRNA in rat hypothalamus during stress

目的 观察应激时大鼠下丘脑血管紧张素原 m RNA表达及血管紧张素 含量的变化 .方法 雄性大鼠 48只随机分为 3组 ,游泳组予以 4℃～ 6℃冷水游泳刺激 ;电击组予以0 .5～ 2 Hz,6 0～ 10 0 V足底电刺激 ,每日 2次 ,每次 2 h,持续1wk;对照组不予任何刺激 .用原位杂交技术及放免分析法检测不同应激时大鼠下丘脑血管紧张素原 (Ang) m RNA的表达及血管紧张素 (Ang )含量的变化 .结果 应激大鼠下丘脑 Ang m RNA阳性表达面积百分比与积分吸光度均显著增高 .游泳组 (2 .48± 0 .40 ) %与 (0 .75± 0 .0 9) ,电击组 (2 .94± 0 .82 ) %与 (1.83± 0 .41) vs对照组 (0 .2 0± 0 .0 4) %与 (0 .2 4± 0 .12 ) ,P<0 .0 1;Ang 含量也显著增高 .游泳组 (141±6 7) ng· g- 1 ,电击组 (84± 2 5 ) ng· g- 1 vs对照组 (5 6± 16 ) ng· g- 1 ,P<0 .0 1,P<0 .0 5 ,且 Ang m RNA表达增高率 (12 16± 196 ) %和 (144 1± 40 2 ) % ,超过了 Ang 含量的增高率(2 95± 118) %和 (149± 44 ) % ,P<0 .0 1.结论 应激时下丘脑肾素 -血管紧张素系统 (RAS)被显著激活 ,进一步支持局部RAS参与了应激反应的观点 .

AIM To investigate the expression of angiotensinogen (Ang) mRNA and the changes of angiotensin Ⅱ(AngⅡ) contents in rat hypothalamus during stress. METHODS Forty eight male rats were randomly allocated to three groups. Swimming rats were treated with swimming stimulation in 4℃~6℃ cold water; electric shock rats were treated with repetitive 0.5~2 Hz, 60~100 V electric shock on foot for 1wk,twice a day for 2 h each time; and control rats weren't treated with any stimulation. Then Ang mRNA expression in hypothalamus was determined by using in situ hybridization technique, and AngⅡ contents were detected by RIA. RESULTS The area percentage and integral absorbance of Ang mRNA positive expression were significantly increased [swimming group (2.48±0.40)% and (0.75± 0.09 ), electric shock group (2.94±0.82)% and (1.83± 0.41 ), vs control group (0.20±0.04)% and (0.24±0.12), P <0.01], AngⅡ contents were also significantly increased [swimming group (141±67) ng·g -1 , electric shock group (84±25) ng·g -1 , vs control group (56±16) ng·g -1 , P < 0.01 , P <0.05], and the increased rates of Ang mRNA [(1216±196)% and (1441±402)%] surpassed the ones of AngⅡ contents [(295±118)% and (149±44)%] ( P < 0.01 ). CONCLUSION The local renin angiotensin system (RAS) in hypothalamus is obviously activated during stress, which strongly supports the view that local RAS contributes to stress reaction.