What is the primary mechanism of action of phosphodiesterase-5 (PDE-5) inhibitors?

The primary mechanism of action of phosphodiesterase-5 (PDE-5) inhibitors is to enhance the effect of nitric oxide. These medications work by inhibiting the PDE-5 enzyme, which is responsible for the breakdown of cyclic guanosine monophosphate (cGMP). Under normal circumstances, when nitric oxide is released in the penis during sexual stimulation, it promotes the production of cGMP. This molecule is crucial for relaxation of smooth muscle and dilation of blood vessels, leading to increased blood flow and facilitating an erection.

When PDE-5 is inhibited, cGMP levels remain elevated longer, thus prolonging and enhancing its effects. This mechanism specifically targets the pathways involved in erectile function, making PDE-5 inhibitors effective treatments for erectile dysfunction.

In contrast, the other options do not accurately represent the action of PDE-5 inhibitors. For instance, increasing prostaglandin production does not occur directly through this class of drugs, and causing vasoconstriction contradicts the overall goal of these medications, which is to induce vasodilation and improve blood flow. Additionally, antagonizing cyclic GMP would counteract its beneficial effects, rather than enhancing them, leading to a misunderstanding of the drug’s action. The correct understanding