Vardenafil (Vivanza) is an oral therapy for the treatment of erectile dysfunction. It is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Penile erection is a hemodynamic process initiated by the relaxation of smooth muscle in the corpus cavernosum and its associated arterioles. During sexual stimulation, nitric oxide is released from nerve endings and endothelial cells in the corpus cavernosum. Nitric oxide activates the enzyme guanylate cyclase resulting in increased synthesis of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the corpus cavernosum. The cGMP in turn triggers smooth muscle relaxation, allowing increased blood flow into the penis, resulting in erection. The tissue concentration of cGMP is regulated by both the rates of synthesis and degradation via phosphodiesterases (PDEs). The most abundant PDE in the human corpus cavernosum is the cGMPspecific phosphodiesterase type 5 (PDE5); therefore, the inhibition of PDE5 enhances erectile function by increasing the amount of cGMP.

PDE5:0.7 nM

Vardenafil通过依赖于线粒体K（ATP）通道开放机制,防止再灌注损伤的心肌缺血. 口服3 mg/kg Vardenafil导致大鼠中对象识别能力的改变. 口服30 mg / L Vardenafil同时增加大鼠中iNOS和增殖细胞核抗原表达（SM细胞的复制）,伴随动态海绵体融合下降率和SM/胶原蛋白比例的正常化.在兔的心脏中,Vardenafil通过打开线粒体K（ATP）通道诱导缺血/再灌注损伤强大的预处理般的心脏保护作用.Vardenafil在兔子体内剂量依赖性诱导静脉注射Nitroprusside钠盐引起的勃起反应.

Vardenafi能够明显诱导乙酰胆碱和电刺激诱发的小梁平滑肌的放松。Vardenafil, tadalafil和Sildenafil竞争性抑制cGMP的水解磷酸二酯酶5,从而促进血管平滑肌中的环鸟苷酸的积累和松弛。VardenafilI C50是0.7 nM(6.6 nM)时特异性抑制PDE5介导cGMP的水解。Vardenafi在3 nM（10 nM）明显提高了SNP诱导的人小梁平滑肌的松驰。100 mM Vardenafil显著增加大鼠海马环鸟苷酸的水平。