首页> 外文期刊>The journal of sexual medicine >Losartan, an Angiotensin type I receptor, restores erectile function by downregulation of cavernous renin-angiotensin system in streptozocin-induced diabetic rats.
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Losartan, an Angiotensin type I receptor, restores erectile function by downregulation of cavernous renin-angiotensin system in streptozocin-induced diabetic rats.

机译:Losartan是一种I型血管紧张素受体,可通过下调链脲佐菌素诱导的糖尿病大鼠的海绵状肾素-血管紧张素系统恢复勃起功能。

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INTRODUCTION: The high incidence of erectile dysfunction (ED) in diabetes highlights the need for good treatment strategies. Recent evidence indicates that blockade of the angiotensin type I receptor (AT1) may reverse ED from various diseases. AIM: To explore the role of cavernous renin-angiotensin system (RAS) in the pathogenesis of diabetic ED and the role of losartan in the treatment of diabetic ED. METHODS: The AT1 blocker (ARB) losartan (30 mg/kg/d) was administered to rats with streptozocin (65 mg/kg)-induced diabetes. Erectile function, cavernous structure, and tissue gene and protein expression of RAS in the corpora cavernosa were studied. MAIN OUTCOME MEASURE: We sought to determine the changes of cavernous RAS in the condition of diabetes and after treatment with losartan. RESULTS: RAS components (angiotensinogen, [pro]renin receptor, angiotensin-converting enzyme [ACE], and AT1) were expressed in cavernosal tissue. In diabetic rats, RAS components were upregulated, resulting in the increased concentration of angiotensin II (Ang II) in the corpora. A positive feedback loop for Ang II formation in cavernosum was also identified, which could contribute to overactivity of cavernous RAS in diabetic rats. Administration of losartan blocked the effect of Ang II, downregulated the expression of AT1 and Ang II generated locally, and partially restored erectile function (losartan-treated group revealed an improved intracavernous pressure/mean systemic arterial pressure ratio as compared with the diabetic group (0.480 +/- 0.031 vs. 0.329 +/- 0.020, P < 0.01). However, losartan could not elevate the reduced smooth muscle/collagen ratio in diabetic rats. CONCLUSIONS: The cavernous RAS plays a role in modulating erectile function in corpora cavernosa and is involved in the pathogenesis of diabetic ED. ARB can restore diabetic ED through downregulating cavernous RAS.
机译:简介:糖尿病中勃起功能障碍(ED)的高发率凸显了对良好治疗策略的需求。最近的证据表明,阻断I型血管紧张素受体(AT1)可能使ED逆转各种疾病。目的:探讨海绵状肾素-血管紧张素系统(RAS)在糖尿病性ED发病中的作用以及氯沙坦在糖尿病性ED治疗中的作用。方法:对链脲佐菌素(65 mg / kg)诱导的糖尿病大鼠给予AT1阻滞剂(ARB)氯沙坦(30 mg / kg / d)。研究了海绵体的勃起功能,海绵体结构以及RAS的组织基因和蛋白质表达。主要观察指标:我们试图确定在糖尿病情况下和氯沙坦治疗后海绵状RAS的变化。结果:RAS成分(血管紧张素原,肾素原受体,血管紧张素转换酶[ACE]和AT1)在海绵体组织中表达。在糖尿病大鼠中,RAS成分上调,导致语料库中血管紧张素II(Ang II)的浓度增加。还确定了海绵体中Ang II形成的正反馈回路,这可能导致糖尿病大鼠海绵体RAS过度活跃。氯沙坦的给药可阻断Ang II的作用,下调局部产生的AT1和Ang II的表达,并部分恢复勃起功能(氯沙坦治疗组显示,与糖尿病组相比,海绵体内压力/平均全身动脉压比有所改善(0.480 +/- 0.031与0.329 +/- 0.020,P <0.01),但是,氯沙坦不能提高糖尿病大鼠平滑肌/胶原蛋白比例的降低。结论:海绵体RAS在调节海绵体和海绵体中的勃起功能中起一定作用糖尿病ED的发病机制涉及ARB可以通过下调海绵状RAS而恢复糖尿病ED。

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