Dai Yu-Tian, Mills Thomas M, Lewis Ronald W, Webb R Clinton
Department of Urology, Affiliated Drum Tower Hospital, Nanjing University School of Medicine, Nanjing, Jiangsu 210008, China.
Zhonghua Nan Ke Xue. 2002 Dec;8(6):391-4.
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 occurred 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 hypertension, 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.
研究表明,海绵体循环中的血管收缩是由RhoA/Rho激酶钙敏化途径介导的。用Y-27632抑制海绵体平滑肌中的Rho激酶活性会导致勃起反应,其特征是海绵体内压(ICP)升高,而男性动脉压(MAP)无显著变化。为了解释在这种强烈的血管收缩信号存在的情况下如何发生勃起,我们推测一氧化氮(NO)通过直接抑制RhoA/Rho激酶途径的活性来诱导血管舒张从而导致勃起,从而减少血管收缩。给予Y-27632可恢复性腺功能减退和高血压大鼠模型的勃起功能,这表明抑制Rho激酶可能具有潜在的临床价值。此外,我们的结果表明,局部应用Y-27632可能是治疗勃起功能障碍的有效方式。