摘要
目的 :观察卡托普利对压力负荷性心肌肥厚大鼠心肌组织中的血管紧张素 (MAng )及一氧化氮合成酶 (NOS)含量的影响。方法 :本实验采用腹主动脉缩窄法建立大鼠压力负荷性心肌肥厚模型 ,用放免法测定 MAng 及比色法测定 NOS含量。结果 :腹主动脉缩窄后 4周 ,心脏重量与 MAng 含量显著增加 ,NOS也代偿性增加 ,而血浆 Ang (PAng )变化不明显 ;卡托普利能降低全心重 /体重比值 ,增加 NOS活性 ,降低MAng 含量。结论心脏肾素 -血管紧张素系统 (RAS)与NO/NOS系统参与了心肌肥厚的发生发展 。
Aim:To investigate the effect of captopril on the myocardium angiotensinⅡ (MAngⅡ) and nitric oxide synthase (NOS) in rats with pressure overload cardiac hypertrophy. Methods: The pressure overload cardiac hypertrophy model was produced by constriction of abdominal aorta. MAngⅡ was measured by radioimmunoassay, and NOS by colorimetric method. Results:Four weeks after abdominal aorta constriction, the ratio of heart weight to body weight(HW/BW) and the level of MAngⅡ and NOS was increased, but no significant changes in plasma AngⅡ(PAngⅡ) were observed; captopril reduced the HW/BW ratio and the level of MAngⅡ, increased the myocardium NOS. Conclusion:A localized cardiac renin angiotensin system(RAS) and NO/NOS system involved in the cardiac hypertrophy, The reversal of cardiac hypertrophy by captopril was associated with the lowering of MAngⅡ and increase in MNOS.
出处
《高血压杂志》
CSCD
2000年第2期174-175,共2页
Chinese Journal of Hypertension
