论文部分内容阅读
一般认为一氧化氮(nitricoxide,NO)释放增加促进小动脉和海绵体平滑肌舒张是导致男性阴茎勃起的主要机制.研究发现内源性血管收缩因子对维持阴茎萎软状态有重要作用.应用大鼠模型活体检测使用Y 27632拮抗Rho 激酶活性后对阴茎勃起生理机制的影响;应用免疫转印技术检测阴茎海绵体内RhoA和Rho激酶蛋白的表达.结果显示在大鼠海绵体组织内有内源性RhoA和Rho激酶蛋白的表达和存在;Y 27632海绵体内注射阻滞RhoA/Rho激酶活性使ICP和CCP/MAP比值明显升高;局部小剂量应用Y 27632对MAP没有明显影响;Y 27632可增强系列电刺激引起的由NO介导的CCP/MAP比值的增加;NO合成酶和鸟苷酸环化酶抑制剂的作用不能阻滞RhoA/Rho激酶抑制剂对大鼠阴茎海绵体平滑肌的松弛作用和CCP/MAP的增加.说明RhoA/Rho激酶信号系统发挥了维持海绵体萎软状态重要作用,这是与NO介导途径不同的阴茎勃起生理调节机制.RhoA/Rho激酶抑制剂可能是ED治疗的新领域新方法.
It is generally believed that the increase of nitric oxide (NO) release promotes the relaxation of the smooth muscle of the arterioles and cavernosum, which is the main mechanism leading to penile erection in males.It is found that endogenous vasoconstriction factor plays an important role in maintaining the penile atrophy.Application of rat The model was used to detect the effect of Y 27632 on the physiological mechanism of penile erection after Rho kinase activity was detected.The expression of RhoA and Rho kinase in the penis was detected by immunoblotting.The results showed that endogenous RhoA And Rho kinase protein expression and presence; Y 27632 intracavernosal injections RhoA / Rho kinase activity so that the ICP and CCP / MAP ratio was significantly increased; local small doses of Y 27632 MAP had no significant effect; Y 27632 can enhance the series of electricity Stimulated NO-mediated increase in the ratio of CCP / MAP; NO synthase and guanylate cyclase inhibitors did not block the relaxation of RhoA / Rho kinase inhibitors on rat corpus cavernosum smooth muscle and CCP / MAP increase, indicating that the RhoA / Rho kinase signaling system plays an important role in maintaining the sponge wilting state, which is different from the NO-mediated erectile dysfunction Mechanism .RhoA / Rho kinase inhibitor may be a new field of a new method of treating ED.