A. Phosphodiesterase Inhibitors
Three phosphodiesterase-5 (PDE5) inhibitors, sildenafil (Viagra), vardenafil (Levitra), and tadalafil (Cialis) have been approved and are effective in a broad population of men with ED. PDE5 inhibitors cause improvement of ED by preventing the breakdown of cyclic GMP, the substance that promotes relaxation of smooth muscle cells in the arteries, arterioles, and sinusoids of the corpus cavernosum of the penis. Phosphodiesterases are enzymes that hydro-lyze cGMP, a prime mediator of vasodilation. Sildenafil, a phosphodiesterase inhibitor, has a high affinity for the phosphodiesterase-5 (PDE-5) isoform that is abundant in the corpus cavernosum vascular smooth muscle, visceral and skeletal muscle, and in platelets. Figure 1 indicates both the normal physiology of penile erection and that inhibition of PDE-5 causes accumulation of cGMP. This accumulation produces arterial dilatation and increased blood flow to the corpus cavernosal smooth muscle. The exact mechanism for penile smooth muscle relaxation following NO-induced cGMP accumulation and the veno-occlusive phenomenon which causes entrapment of blood that maintains engorgement and sustains the erection remain unclear (Fig. 1).

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