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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 role of angiotensin Ⅱ (Ang Ⅱ) and its type 1 receptor (AT1) in the pathogenesis of diabetic erectile dysfunction (DED). Methods The whole experiment is divided into two parts. The first part of the experiment in the rat model of diabetes mellitus after feeding for 8 weeks, screened erectile dysfunction rats, all the rats were divided into 3 groups: normal group, diabetic group (DM), DED group. The rats in the 3 groups were anesthetized and the inferior vena cava was taken for blood. The penile tissues were taken for immunohistochemical observation of the changes of the distribution of AngⅡreceptors and the level of AngⅡ in tissue homogenate and blood by radioimmunoassay. The second part of the experiment in diabetic rat model was established, immediately divided into three groups: diabetic untreated group, valsartan group, spironolactone group. After 8 weeks of treatment, erectile function was evaluated by apomorphine screening and intracavernous pressure measurement respectively. Results Compared with the control group, the levels of AngⅡ in the blood and sponge tissues and DED group were significantly increased (P <0.05), while the levels of Ang Ⅱ in the penis tissue of DED group were significantly increased (P <0.001). The distribution of AngⅡreceptor in the penile tissue of rats in each group decreased with the increase of AngⅡ. After 8 weeks of valsartan treatment, compared with the untreated group and spironolactone group, the former erectile rate and sponge pressure were significantly increased. Conclusion Ang Ⅱ may play a role in the pathogenesis of DED. Angiotensin receptor angiotensin AT1 antagonist may be one of the important methods for the future treatment of DED.