Overview of phosphodiesterase 5 inhibition in erectile dysfunction

Am J Cardiol. 2003 Nov 6;92(9A):9M-18M. doi: 10.1016/s0002-9149(03)00824-5.

Abstract

Since the early 1980s, research on the mechanisms of penile erection has done much to clarify erectile physiology and pathophysiology. More recent studies have identified the importance of neurochemical mediators in erection. These include the nitric oxide-cyclic guanosine monophosphate (cGMP) cell-signaling system-a complex molecular pathway that mediates smooth muscle relaxation in the corpus cavernosum. Phosphodiesterase 5 (PDE5) inactivates cGMP, which terminates nitric oxide-cGMP-mediated smooth muscle relaxation. Inhibition of PDE5 is expected to enhance penile erection by preventing cGMP degradation. Development of pharmacologic agents with this effect has closely paralleled the emerging science. The prototype of this new therapeutic class of PDE5 inhibitors is sildenafil, which was approved for treatment of erectile dysfunction in 1998. Tadalafil and vardenafil are new agents in this class. These agents have demonstrated improvement in erectile function and have been shown to be well tolerated in diverse populations comprising thousands of men worldwide. Profiles of these 3 PDE5 inhibitors are reviewed herein.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • 3',5'-Cyclic-GMP Phosphodiesterases / antagonists & inhibitors*
  • Carbolines / pharmacology
  • Erectile Dysfunction / drug therapy*
  • Humans
  • Imidazoles / pharmacology
  • Male
  • Phosphodiesterase Inhibitors / chemistry
  • Phosphodiesterase Inhibitors / pharmacology*
  • Piperazines / pharmacology
  • Purines
  • Sildenafil Citrate
  • Sulfones
  • Tadalafil
  • Triazines
  • Vardenafil Dihydrochloride

Substances

  • Carbolines
  • Imidazoles
  • Phosphodiesterase Inhibitors
  • Piperazines
  • Purines
  • Sulfones
  • Triazines
  • Vardenafil Dihydrochloride
  • Tadalafil
  • Sildenafil Citrate
  • 3',5'-Cyclic-GMP Phosphodiesterases