Description

Initially studied as a cure for angina pectoris, during tests it showed little efficacy in this sense while the main evidence was related to side effects, the main of which was the appearance of an erection.

Patented in 1996 and approved by the FDA as a drug against erectile dysfunction, on March 27 1998, it also opened the market to equivalent medicines containing the same principle.

The phenomenon of erection is due to a relaxation of the smooth muscles of the corpus cavernosum of the penis which is followed by arterial vasodilation. The parallel constriction of the venous vessels causes stagnation of blood which follows an erection. Relaxation of the smooth muscles of the corpus cavernosum is a phenomenon mediated by nitric oxide (NO). It activates the enzyme guanylate cyclase which catalyzes the transformation of guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP) which stimulates muscle relaxation. The cGMP is degraded by a phosphodiesterase of which at least 11 isoenzymes are known. In the corpus cavernosum, the phosphodiesterase involved is phosphodiesterase type 5 (5PDE).

Sildenafil works by inhibiting 5PDE, which causes an increase in blood supply, following an increase in the concentration of cGMP, followed by an improvement in erection. At therapeutic dosages, sildenafil does not produce erection in the absence of sexual stimulation.

The recommended dosage is half a tablet, 40-60 minutes before intercourse.

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