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Tadalafil is a particular phosphodiesterase type 5 (PDE5) cyclic guanosine monophosphate (cGMP) inhibitor that is reversible, powerful, and selective. Tadalafil increases cGMP levels in the corpora cavernosa by inhibiting PDE5, which causes nitric oxide to be released locally in response to sexual stimulation. The smooth muscle relaxes as a result, allowing blood to flow to the penile tissues and causing an erection. Without sexual excitement, tadalafil has no effect.
Tadalafil has been demonstrated to be a selective PDE5 inhibitor in in vitro tests. Smooth muscle in the penile corpora cavernosa, vascular and visceral smooth muscle, skeletal muscle, platelets, kidney, lung, and cerebellum all contain the enzyme PDE5. Tadalafil has a more focused action on PDE5 than on other phosphodiesterases. When compared to PDE1, PDE2, PDE4, and PDE7 enzymes found in the heart, brain, blood arteries, liver, leukocytes, skeletal muscle, and other organs, tadalafil is 10,000 times more selective for PDE5. PDE5, an enzyme present in the heart and blood arteries, is >10,000 times more selective for tadalafil than PDE3. This is significant since PDE3 is an enzyme involved in cardiac contractility, and PDES has a better selectivity than PDE3. Additionally, tadalafil is around 700 times more selective for the phototransduction enzyme PDE5 than for PDE6, which is present in the retina. Additionally, tadalafil is 14 times more selective for PDE5 than PDE11 and >9,000 times more selective for PDE5 than PDE8, PDE9, and PDE10. PDE8 to PDE11 inhibition’s tissue distribution and physiological effects are still poorly understood.