What are oral therapies for ED specifically the phosphodiesterase type 5 PDE5 inhibitors

Currently, three oral therapies are available for the treatment of ED. The first therapy to become available was sildenafil (Pfizer's Viagra), which was approved by the FDA in 1998. Vardenafil (Bayer's Levitra) and tadalafil (Lily Icos's Cialis) were approved for use years later. All three of these oral therapies are phosphodi-esterase type 5 (PDE-5) inhibitors.

To understand how these therapies work, it is important to review the process involved in the normal erection. When aroused or stimulated sexually, the brain sends messages from nerves in the pelvis, resulting in the release of nitric oxide. The nitric oxide then stimulates the production of cGMP, which in turn tells the cavernosal muscle in the penis to relax, thereby allowing more blood to flow into the penis. cGMP is broken down in the penis by an enzyme, phosphodiesterase type 5 (PDE-5) (Figure 32). Thus, if PDE-5 is prevented from working by administration of a PDE-5 inhibitor, there will be more cGMP present and thus a greater stimulus for increased blood flow.

Critical to the success of all of the PDE-5 inhibitors is the need for sexual arousal (sexual stimulation) after taking the medication. That is, these medications will not cause an erection to occur without sexual stimulation. It is okay to have a glass of wine, a beer, or a mixed drink when using these therapies—such limited alcohol consumption should not interfere with their effectiveness. Too much alcohol, however, may have a negative effect on erectile function, so a man should limit his alcohol intake when taking any of these medications.

Figure 32 Neurologic mechanism of erectile function. Sexual stimulation leads to release of nitric oxide, which leads to an increase in cGMP, a neurotransmitter that causes smooth muscle relaxation and increased blood flow into the penis. Abbreviations within the figure are: cGMP, cyclic guanosine monophosphate; GMP, guanosine monophosphate; GTP, guanosine triphosphate; nanc, nonadrenergic-noncholinergic neurons; CO, nitric oxide; PDES, phosphodiesterase type 5.

Figure 32 Neurologic mechanism of erectile function. Sexual stimulation leads to release of nitric oxide, which leads to an increase in cGMP, a neurotransmitter that causes smooth muscle relaxation and increased blood flow into the penis. Abbreviations within the figure are: cGMP, cyclic guanosine monophosphate; GMP, guanosine monophosphate; GTP, guanosine triphosphate; nanc, nonadrenergic-noncholinergic neurons; CO, nitric oxide; PDES, phosphodiesterase type 5.

Reprinted with permission from AmJ Cardiol 1999; 84(5B):11N-17N.

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