摘要
目的 观察血管紧张素原 (AGT)及血管紧张素Ⅱ 1型受体 (AT1 )蛋白表达改变是否参与模拟失重所致大鼠不同部位动脉血管的分化性适应过程。 方法 以尾部悬吊大鼠模型模拟失重对动脉血管的影响。用Western印迹分析比较 4周模拟失重 (SUS)组与同步对照 (CON)组大鼠基底动脉、颈总动脉、股动脉和肠系膜动脉组织AGT及AT1 的蛋白表达变化。 结果 与CON组相比 ,SUS组大鼠基底动脉组织AGT的表达显著增高 (P <0 .0 5 ) ,在颈总动脉组织呈增高趋势 ,而在股动脉与肠系膜动脉组织均呈降低趋势 ,但差别皆未达到显著水平。与CON组相比 ,SUS组大鼠基底动脉组织AT1 的表达显著增高 (P <0 .0 5 ) ,在颈总动脉组织未见显著变化 ,而在股动脉和肠系膜动脉组织则均显著降低 (P <0 .0 5 )。 结论 模拟失重可引起大鼠脑动脉与后身动脉血管组织的AGT和AT1 蛋白表达发生增高与降低的分化性改变 ,提示血管组织的局部肾素 血管紧张素系统在失重引起的动脉血管分化性适应中可能发挥关键性的调控作用。
Objective To determine whether the changes of both angiotensinogen (AGT) and angiotensin Ⅱ type 1 receptor (AT 1) protein expression are involved in differential adaptation of arteries induced by simulated weightlessness in rats. Methods Tail suspension rat model was used to simulate the effects of weightlessness on vessels. The protein expression of AGT and AT 1 in basilar, carotid, femoral, and mesenteric arterial tissues were demonstrated by Western blotting and normalized by β actin for quantitative comparison. Results After 4 wk simulated weightlessness, the protein level of AGT in basilar arterial tissue of SUS group was significantly increased ( P < 0.05 ) as compared with that of the CON group; but it showed only a general trend of increase statistically non significant in carotid and a trend of decrease in femoral and mesenteric arterial tissues as compared with those of CON group. Compared with the CON group, the protein expression of AT 1 in basilar arterial tissue was significantly increased ( P <0.05); and in femoral and mesenteric arterial tissues was significantly decreased ( P <0.05). However, no significant change was noted in carotid arterial tissue. Conclusions The protein expression of AGT and AT 1 is up and down regulated in cerebral and hindquarter arterial tissues respectively in tail suspended rats. These findings further suggest that local renin angiotensin system may play a pivotal role in the differential adaptation of vessels to microgravity.
出处
《中华航空航天医学杂志》
CSCD
2003年第1期1-4,共4页
Chinese Journal of Aerospace Medicine
基金
国家自然科学基金 ( 3 0 1710 3 2 )
全军医药卫生科研基金 ( 0 1MB12 2 )资助项目