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血管活性肠肽,一种勃起神经递质,在去势大鼠中比在正常大鼠中更显著地改善勃起功能。

Vasoactive intestinal polypeptide, an erectile neurotransmitter, improves erectile function more significantly in castrated rats than in normal rats.

机构信息

Department of Urology, Ruijin Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, PR China.

出版信息

BJU Int. 2011 Aug;108(3):440-6. doi: 10.1111/j.1464-410X.2010.09901.x. Epub 2010 Dec 16.

Abstract

OBJECTIVE

• 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.

MATERIALS AND METHODS

• 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.

RESULTS

• 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.

CONCLUSION

• 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.

摘要

目的

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。

材料和方法

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。

结果

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。

结论

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。

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