What is Sildenafil Citrate

Q. What is Sildenafil Citrate?

Generic Sildenafil Citrate is the active ingredient used to treat erectile dysfunction (impotence) in men. It can help men who have erectile dysfunction get and sustain an erection when they are sexually excited. One does not get an erection just by taking this medicine. Generic Sildenafil Citrate helps a man with erectile dysfunction get an erection only when he is sexually excited.

Q. How does Sildenafil Citrate work?

Generic Sildenafil Citrate enables many men with ED to respond to sexual stimulation. When a man is sexually aroused, the arteries in the penis relax and widen, allowing more blood to flow into the penis. As the arteries in the penis expand and harden, the veins that normally carry blood away from the penis become compressed, restricting the blood flow out of the penis. With more blood flowing in and less flowing out, the penis enlarges, resulting in an erection. Sildenafil inhibits the production of the PDE5 phosphate that is responsible for keeping the penis limp. Please understand that Generic Sildenafil Citrate is not a hormone or aphrodisiac, it works only when a man is sexually stimulated.

Remember that no medicine is for everyone. If you use nitrate drugs, often used to control chest pain (also known as angina), don't take sildenafil citrate. This combination could cause your blood pressure to drop to an unsafe or life-threatening level. Be sure to ask your doctor if your heart is healthy enough for sexual activity. For most patients, the recommended dose is 50 mg taken, as needed, approximately 1 hour before sexual activity. However, the dose may be taken anywhere from 4 hours to 0.5 hour before sexual activity. Based on effectiveness and toleration, the dose may be increased to a maximum recommended dose of 100 mg or decreased to 25 mg. The maximum recommended dosing frequency is once per day.

Mechanism of Action

The physiologic mechanism of erection of the penis involves release of nitric oxide (NO) in the corpus cavernosum during sexual stimulation. NO then activates the enzyme guanylate cyclase, which results in increased levels of cyclic guanosine monophosphate (cGMP), producing smooth muscle relaxation in the corpus cavernosum and allowing inflow of blood. Sildenafil has no direct relaxant effect on isolated human corpus cavernosum, but enhances the effect of nitric oxide (NO) by inhibiting phosphodiesterase type 5 (PDE5), which is responsible for degradation of cGMP in the corpus cavernosum. When sexual stimulation causes local release of NO, inhibition of PDE5 by sildenafil causes increased levels of cGMP in the corpus cavernosum, resulting in smooth muscle relaxation and inflow of blood to the corpus cavernosum. Sildenafil at recommended doses has no effect in the absence of sexual stimulation.

Studies in vitro have shown that sildenafil is selective for PDE5. Its effect is more potent on PDE5 than on other known phosphodiesterases (80-fold for PDE1, 1000-fold for PDE2, PDE3, and PDE4). The approximately 4000-fold selectivity for PDE5 versus PDE3 is important because that PDE is involved in control of cardiac contractility. Sildenafil is only about 10-fold as potent for PDE5 compared to PDE6, an enzyme found in the retina; this lower selectivity is thought to be the basis for abnormalities related to color vision observed with higher doses or plasma levels (see Pharmacodynamics).

In addition to human corpus cavernosum smooth muscle, PDE5 is also found in lower concentrations in other tissues including platelets, vascular and visceral smooth muscle, and skeletal muscle. The inhibition of PDE5 in these tissues may be the basis for the enhanced platelet antiaggregatory activity of nitric oxide observed in vitro, an inhibition of platelet thrombus formation in vivo and peripheral arterial-venous dilatation in vivo.