卡托普利对糖尿病大鼠心肌组织肾素─血管紧张素系统的影响

在链脲霉素所致糖尿病大鼠模型（链脲霉素７０ｍｇ·ｋｇ－１，ｉＰ）观察了大鼠心肌组织肾素血管紧张素系统（ＲＡＳ）的变化以及血管紧张素转换酶抑制剂卡托普利的治疗作用（４．６ｍｍｏｌ·Ｌ－１卡托普利饮水给药４ｗｋ）。结果表明，糖尿病大鼠较正常大鼠心肌组织ＲＡ、ＡＣＥ活性显著升高（Ｐ＜０．０１），ＡｎｇⅠ、ＡｎｇⅡ、ＡＬＤ含量均明显增加（Ｐ＜０．０１）。卡托普利治疗组大鼠较糖尿病大鼠上述各项指标均有不同程度的降低，其中ＡＣＥ活性和ＡｎｇⅠ、ＡＭⅡ含量的改变有显著性差异（Ｐ＜０．０５，Ｐ＜０．０１），ＲＡ和ＡＬＤ含量改变差异无显著性（Ｐ＞０．０５）。提示：心肌组织ＲＡＳ功能亢进参与了糖尿病性心肌病发病过程。卡托普利对心肌组织ＲＡＳ的抑制作用可能是其减轻糖尿病心肌损害的主要作用机制。

Effect of captopril on the myocardial renin-angiotensin system in streptozotocin diabetic rats

Change of myocardial renin-angiotensin system and effects of angiotensin convertingenzyme inhibitor captoril(water with 4.6 mmol·L-1 captopril drunk for 4 weeks) were studied in streptozotocin induced diabetic rats(streptozotocin 70mg·kg-1,ip,bolus injection).The activities of renin and ACE significantly increased in diabetic rats compared with the normal rats(P<0.01),so did the contents of the Aug Ⅰ,AugⅡ and ALD in the myocardium (P<0.01).The activity of ACE and contents of AngⅠ,AngⅡin the myocardium significantly decreased in captopril treated rats compared with the diabetic rats(P<0.05,P<0.01),but renin and ALD were not different in the two groups(P>0.05).It was supposed that the hyperfunction of myocardial RAS had effects on the pathogenesis of diabetic cardiomyopathy,and that the inhibition of the myocardial RAS might be one of the mechanisms of captopril's effect on relieving diabetic myocardial damage.