Sildenafil citrate is a selective 5-phosphodiesterase inhibitor that enhances nitric oxide-dependent, cyclic guanosine monophosphate-mediated pulmonary vasodilation by inhibiting the breakdown of cyclic guanosine monophosphate. In addition to the direct expansion of pulmonary blood vessels, it can also prevent or reverse vascular remodeling.

Sildenafil citrate, trade name Viagre, commonly known as Viagra, is a cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5) inhibitor that can enhance erection after oral administration. Sildenafil citrate can enhance the effect of nitric oxide (NO) by inhibiting the type 5 phosphodiesterase that decomposes cyclic guanosine monophosphate (cGMP) in the corpus cavernosum. Increase the level of cGMP in the corpus cavernosum, relax the smooth muscle in the corpus cavernosum, increase the inflow of blood, prolong the penis erection time and increase the firmness. For impotence patients with erectile dysfunction. Adults take 50 mg orally each time, up to 1 time a day, and use it as needed about 1 hour before sexual intercourse. The maximum amount is 0.1g each time.

In anesthetized dogs, Sildenafil citrate enhances penile erectile function under pelvic nerve stimulation by measuring intracavernous pressure. Sildenafil citrate markedly reversed impaired carbamoylcholine-stimulated relaxation and inhibited superoxide formation in the cavernosal tissue of hypercholesterolemic rabbits. In Sprague-Dawley rats, Sildenafil improves erectile function in a time-dose-dependent manner, with maximal recovery occurring on day 28 at a dose of 20 mg/kg per day. In Sprague-Dawley rats, administration of Sildenafil resulted in smooth muscle collagen ratio preservation and preservation of CD31 and eNOS expression. In Sprague-Dawley rats, Sildenafil significantly reduced the apoptotic index and increased the phosphorylation of akt and eNOS compared with the control group.