Department of Urology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.
BJU Int. 2011 Aug;108(3):440-6. doi: 10.1111/j.1464-410X.2010.09901.x. Epub 2010 Dec 16.
• To investigate the regulatory role of androgen in VIP-mediated erectile effect. Androgen is essential for physiological erection. Vasoactive intestinal polypeptide (VIP) is an important erectile neurotransmitter. While previous studies demonstrated that VIP expression in the penis was androgen-independent, it remains controversial whether androgen has any effect on VIP-mediated erection.
• Male SD rats were divided into a control group, a castration group, and a castration-with-testosterone-replacement group. Four weeks later, each group was subdivided into low and high-dose VIP subgroups and subjected to intracavernous injection of 0.5 and 2 µg VIP, respectively. • Erectile function was tested by recording intracavernosal pressure (ICP) and mean arterial blood pressure (MAP) before and after VIP injection. • The expressions of the VIP-receptor (VPAC2), G-protein stimulatory and inhibitory alpha subunits (Gs-α, Gi-α), and PDE3A in rat corpus cavernosum (CC) was qualified by real-time PCR and Western blot analysis.
• Castration reduced erectile function while testosterone restored it. VIP improved erectile function in a dose-dependent manner. • High-dose VIP significantly enhanced erectile function in castrated rats and there was no difference of ICP/MAP among three groups after injection of high-dose VIP. • Low-dose VIP also resulted in a higher improvement of erectile function in castrated rats, although the ICP/MAP was lower in these rats than in the other two groups. VPAC2 and Gs-α were up-regulated while Gi-α and PDE3A were down-regulated in CC of castrated rats.
• VIP improves erectile function much more significantly in hypogonadal condition, mainly due to the higher expression of VPAC2, Gs-α, and lower expression of Gi-α and PDE3A in CC of castrated rats. Androgen may negatively regulate the erectile effect of VIP.
探讨雄激素在 VIP 介导的勃起效应中的调节作用。雄激素对生理勃起至关重要。血管活性肠肽（VIP）是一种重要的勃起神经递质。虽然之前的研究表明阴茎中 VIP 的表达与雄激素无关，但雄激素是否对 VIP 介导的勃起有影响仍存在争议。
雄性 SD 大鼠分为对照组、去势组和去势加睾酮替代组。四周后，每组再分为低剂量 VIP 亚组和高剂量 VIP 亚组，分别给予 0.5 和 2μg VIP cavernous 内注射。通过记录注射 VIP 前后 cavernous 内压（ICP）和平均动脉压（MAP）来测试勃起功能。采用实时 PCR 和 Western blot 分析鉴定大鼠海绵体（CC）中 VIP 受体（VPAC2）、G 蛋白刺激和抑制α亚单位（Gs-α、Gi-α）和 PDE3A 的表达。
去势降低了勃起功能，而睾酮则恢复了勃起功能。VIP 以剂量依赖的方式改善勃起功能。高剂量 VIP 可显著增强去势大鼠的勃起功能，且三组大鼠注射高剂量 VIP 后 ICP/MAP 无差异。低剂量 VIP 也可显著改善去势大鼠的勃起功能，尽管这些大鼠的 ICP/MAP 低于其他两组。CC 中 VPAC2 和 Gs-α 上调，而 Gi-α 和 PDE3A 下调。
VIP 在去势状态下改善勃起功能的效果更为显著，主要是由于去势大鼠 CC 中 VPAC2、Gs-α 的表达增加，而 Gi-α 和 PDE3A 的表达降低。雄激素可能负调节 VIP 的勃起效应。
