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An agent for the treatment of erectile dysfunction, is a reversible selective inhibitor of specific PDE5 cGMP. When sexual arousal induces a local release of nitric oxide, inhibition of PDE5 by tadalafil leads to an increase in cGMP levels in the corpus cavernosum of the penis. The consequence of this is relaxation of the smooth muscles of the arteries and blood flow to the tissues of the penis, which causes an erection. Tadalafil is ineffective in the absence of sexual stimulation.

As for its direct profile functions, Cialis improves erection and increases the quality and usefulness of sexual intercourse. True, a prerequisite for the implementation of this effect by the drug is sexual stimulation. For patients who are less active on the love front, a one-time intake of Cialis is recommended immediately before intercourse at a dose of 20 mg (this dose is also the maximum).

In vitro studies have shown that tadalafil is a selective PDE5 inhibitor. PDE5 is an enzyme found in the smooth muscles of the corpora cavernosa, in the smooth muscles of the vessels of the internal organs, in skeletal muscles, platelets, kidneys, lungs, and cerebellum. The effect of tadalafil on PDE5 is more active than on other phosphodiesterases. Tadalafil is 10,000 times more active against PDE5 than against PDE1, PDE2, PDE4, which are localized in the heart, brain, blood vessels, liver and other organs. Tadalafil is 10,000 times more active in blocking PDE5 than PDE3, an enzyme found in the heart and blood vessels. This selectivity for PDE5 over PDE3 is important because PDE3 is an enzyme involved in cardiac muscle contraction. In addition, tadalafil is approximately 700 times more active against PDE5 than against PDE6, which is found in the retina and is responsible for phototransmission. Tadalafil is also 10,000 times more active against PDE5 compared to its effect on PDE7-PDE10.