摘要
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。
It has shown that vasoconstriction in the cavernosal circulation is mediated by the RhoA/Rho kinase calcium sensitization pathway. Inhibition of Rho kinase activity in cavernosal smooth muscle with Y 27632 resulted in an erectile response marked by elevated intracavernosal pressure (ICP) without a significant change in men arterial pressure (MAP). To explain how erection can occure in the presence of this strong vasoconstrictive signal, we have hypothesized that nitric oxide (NO) induces vasodilation leading to erection by directly inhibiting activity of the RhoA/Rho kinase pathway, thereby reducing vasoconstriction. Administration of Y 27632 restored erectile function in rat models of hypogonadism and hypertention, suggesting that Rho kinase inhibition may have potential clinical value. In addition, our results show that topical application of Y 27632 may be an effective mode of treatment for erectile dysfunction.
出处
《中华男科学杂志》
CAS
CSCD
2002年第6期391-394,共4页
National Journal of Andrology
基金
江苏省 13 5工程人才基金
2 0 0 0年国际勃起功能障碍研究学会 (ISIR)青年研究基金资助
