Sildenafil

Sildenafil is a selective inhibitor of phosphodiesterase-5 (PDE5) [1].
Phosphodiesterases (PDEs) are enzymes that hydrolyzing cyclic nucleotides cAMP and cGMP to their inactive 5’-monofosfatos forms. The PDE5 enzyme is responsible for the hydrolysis of the cGMP, which restores GMP levels [1].
In human umbilical vein endothelial cells (HUVECs), Sildenafil (1 mM/5 h) significantly enhanced NO production, which is ~1.5-fold higher than the effect achieved with insulin (100 nM/1 h) [2].
In male C57BL/6 mice, Sildenafil increased glandular activity of the prostate. The secretory epithelium lining showed tall columnar cells. Moreover, the glandular apical region showed evident secretion vesicles. Also, Sildenafil increased substantially testosterone serum levels [1]. In human corpora cavernosa, Sildenafil inhibited PDE5 with a mean IC50 of 3.9 nM. In 12 patients with erectile dysfunction, Sildenafil enhanced the erectile response, which suggested that PDE5 played an important role in human penile erection. So Sildenafil plays as a new effective treatment for penile erectile dysfunction [3].
References:
[1]. Gomes FO, Carvalho Mda C, Saraiva KL, et al. Effect of chronic Sildenafil treatment on the prostate of C57Bl/6 mice. Tissue Cell, 2014, 46(6): 439-449.
[2]. Mammi C1, Pastore D, Lombardo MF, et al. Sildenafil reduces insulin-resistance in human endothelial cells. PLoS One, 2011, 6(1): e14542.
[3]. Boolell M, Allen MJ, Ballard SA, et al. Sildenafil: an orally active type 5 cyclic GMP-specific phosphodiesterase inhibitor for the treatment of penile erectile dysfunction. Int J Impot Res, 1996, 8(2): 47-52.