血管紧张素Ⅱ与糖尿病性勃起功能障碍相关性研究

Study of the Effects of AngiotensinⅡon the Male Rats with Diabetic Erectile Dysfunction

目的探讨血管紧张素Ⅱ(AngⅡ)及其1型受体(AT1)在糖尿病性勃起功能障碍(DED)发病中的作用。方法整个实验分为两部分。第一部分实验在糖尿病大鼠模型建立后,饲养8周,筛选出有勃起功能障碍大鼠,把所有大鼠分为3组:正常组、糖尿病组(DM)、DED组。3组大鼠麻醉后下腔静脉取血;取阴茎组织,分别用于免疫组化观察AngⅡ受体分布量的变化以及放免法测定组织匀浆和血液中AngⅡ水平。第二部分实验在糖尿病大鼠模型建立后,立即分为3组:糖尿病不治疗组、缬沙坦组、螺内酯组。治疗8周后,分别用阿朴吗啡法筛选和海绵体内压测定方法评价勃起功能。结果与对照组相比,DM组血液和海绵体组织及DED组血液中AngⅡ水平明显升高(P<0．05);DED组阴茎组织中AngⅡ水平显著升高(P <0．001);各组大鼠阴茎组织AngⅡ受体分布随AngⅡ增高而降低。而使用缬沙坦治疗8周后,与不治疗组和螺内酯组对比,前者的勃起率和海绵体内压均有明显的增加。结论AngⅡ在DED的发病中可能具有一定作用。应用血管紧张素AngⅡ受体AT1拮抗剂可能会成为将来治疗DED重要方法之一。

Objective To investigate the changes of angiotensin Ⅱ （Ang Ⅱ） and its receptors （AT1） on the male rates with diabetic erectile dysfunction（DED） so as to study its effects. Methods The research can be divided into two parts. First part： After the models of diabetic rats were induced, they had been fed for 8 weeks. Then the rats with erectile dysfunction were selected from these models. All rats were divided into 3 groups： control, diabetes mellitus（DM） and DED. For each rat, the Ang Ⅱ levels of blood and homogenate prepared from a part of isolated penile tissues were determined respectively, and the Ang Ⅱ receptors of the rest of penile tissues were analyzed through immunohistochemical （IHC） assay. Second part： All rats were divided into three groups after the models of diabetic rats were set up： DM（no treatment）, Valsartan and Spironolactone group. After 8 weeks of treatment, we used emetomorphine （APO） and intracavernous pressure （ICP） to value the improvement of erection of experimental rats. Results Compared with the control group, Ang Ⅱ levels of blood and penile tissue in DM group ,as well as the level of blood in DED group, were very high and differences were significant statistically （P〈0.05）. Ang Ⅱ of tissue in DED increased sharply （P〈0.001）. The receptors of Ang Ⅱ changed oppositely against level of Ang Ⅱ. Compared with the control group, the erection frequency and value of ICP in rats of Valsartan treated group were both increased significantly. Conclusion Ang Ⅱ may play an important role in the pathogenesis of DED, and AT 1 antagonist of the angiotensin-converting enzyme （ACE） may become a therapeutic method for DED in future.