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.
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