Pharmacology

Sep-22-2008

The haemodynamic process of erecting a penis is grounded in the relaxation of smooth muscle in the corpus cavernosum and its allied arterioles. Nitric oxide (NO) is released from the corpus cavernosum’s nerve ends during sexual arousal. This triggers the enxyme guanylate cyclase causing the corpus cavernosum’s cyclic guanosine monophosphate (cGMP) levels to increase. This is what causes relaxation in the smooth muscle and allows freer blood flow into the penis, causing an erect penis. The rate of degradation via cGCP hydrolyzing phosphodiesterases (PDEs) and the rate of synthesis via the guanylate cyclase are the two factors that actually regulates the cGMP level. The cGMP specific phosphodiesterase type 5 (PDE5) is the main PDE in the corpus cavernosum of a human. Buy Levitra Plus

Canadian Vardenafil powerfully improves the effect of endogenous Nitric Oxide, which the corpus cavernosum unleashes during sexual arousal, by regulating PDE5. PDE5 is the enzyme that causes cGMP degradation in the corpus caverosum. The levels of cGMP are boosted in the corpus as a result of the PDE5 inhibition, causing smooth muscle relaxation and freer blood flow to the corpus cavernosum. This is how vardenafil creates the potential for men to respond naturally to sexual stimulation.

Quantitative analysis, outside of a living organism, display vardenafil as a selective inhibitor of PDE5. It has an IC50 of 0.7 nM for human platelet PDE5.

Vardenafils inhibitory effects are powerful on powerful on PDE5 than any other known phosphodiesterases (>1,000-fold more than PDE2, 3, 4, 7, 8, 9, and 10, >300-fold more than PDE11, >130-fold more than PDE1). In the isolated human corpus cavernosum, vardenafil drug causes a rise of cGMP causing muscle relaxation, as tested in vitro.

Cheap Vardenafil gives the conscious rabbit an erect penis, but it depends on endogenous nitric oxide synthesis and is potentiate by nitric oxide donors.