Kamagra
October 14th, 2012
The mechanism of action
of Kamagra
(sildenafil) involves the protection of cyclic guanosine
monophosphate (cGMP) from degradation by cGMP-specific
phosphodiesterase type 5 (PDE5) in the corpus cavernosum.
Nitric oxide (NO) in the corpus cavernosum of the penis
binds to guanylate cyclase receptors, which results in
increased levels of cGMP, leading to smooth muscle
relaxation (vasodilation) of the intimal cushions of the
helicine arteries. This smooth muscle relaxation leads to
vasodilation and increased inflow of blood into the spongy
tissue of the penis, causing an erection.
Kamagra is a potent and selective inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5), which is responsible for degradation of cGMP in the corpus cavernosum. The molecular structure of sildenafil is similar to that of cGMP and acts as a competitive binding agent of PDE5 in the corpus cavernosum, resulting in more cGMP and better erections. Without sexual stimulation, and therefore lack of activation of the NO/cGMP system, sildenafil should not cause an erection. Other drugs that operate by the same mechanism include tadalafil (Cialis) and vardenafil (Levitra).
Kamagra Sildenafil is metabolised by liver enzymes and excreted by both the liver and kidneys. If taken with a high-fat meal, absorption is reduced; the time taken to reach the maximum plasma concentration increases by around one hour, and the maximum concentration itself is decreased by nearly one-third.