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阴茎海绵体血管的收缩及张力的维持是由钙敏感的RhoA/Rho激酶信号传导途径介导的。以Y 2 76 32抑制海绵体平滑肌细胞的Rho激酶信号系统可促进阴茎勃起 ,表现为海绵体内压 (ICP)明显升高 ,而平均动脉压 (MAP)变化不显著。为什么在血管收缩信号很强的情况下性刺激仍能引发阴茎勃起反应 ?我们设想体内一氧化氮 (NO)能直接抑制RhoA/Rho激酶途径的活性 ,减少血管张力 ,促使血管舒张 ,勃起发生 ,使用Y 2 76 32可以恢复性腺功能低下和高血压病动物ED模型的阴茎勃起功能 ,这表明抑制Rho激酶活性药物具有临床应用的前景。此外 ,我们的结果显示阴茎表面使用Rho激酶抑制剂可能为ED治疗的有效方法之一。
Contraction and tension maintenance of the cavernosal blood vessels is mediated by the calcium-sensitive RhoA / Rho kinase signaling pathway. Inhibition of Rho kinase signaling system by Y 2 76 32 in cavernosal smooth muscle cells stimulated penile erection with increased intracapsular pressure (ICP) and no significant change in mean arterial pressure (MAP). Why does stimuli of the vasoconstrictor trigger penile erections even in the presence of strong vasoconstrictor signals? We hypothesize that nitric oxide (NO) in the body can directly inhibit the activity of the RhoA / Rho kinase pathway, decrease vascular tone, promote vasodilation and erection, The use of Y 2 76 32 restores penile erection in hypogonadal and hypertensive animal models of ED, suggesting the promise of clinically useful drugs that inhibit Rho kinase activity. In addition, our results show that the use of Rho kinase inhibitors on the surface of the penis may be one of the effective treatments for ED.