Abstract
It is widely accepted that disorders of the male (uro)genital tract, such as erectile dysfunction (ED) and benign diseases of the prostate (lower urinary tract symptomatology or benign prostatic hyperplasia), can be approached therapeutically by influencing the function of both the vascular and non-vascular smooth muscle of the penile erectile tissue or the transition zone/periurethral region of the prostate, respectively. As a result of the discovery of nitric oxide (NO) and cyclic guanosine monophosphate (GMP) as central mediators of penile smooth muscle relaxation, the use of drugs known to increase the local production of NO and/or elevate the intracellular level of the second messenger cyclic GMP have attracted broad attention in the treatment of ED of various etiologies. Specifically, the introduction of vasoactive drugs, including orally active inhibitors of the cyclic GMP-specific phosphodiesterase (PDE) 5, has offered great advantage in the pharmacotherapy of ED and other diseases of the genitourinary tract. These drugs have been proven efficacious with a fast on-set of action and an improved profile of side-effects. This review summarizes current strategies for the treatment of ED utilizing the application of vasoactive drugs via the oral, transurethral, topical, or self-injection route.
Highlights
Erectile dysfunction (ED) is defined as the consistent inability to attain or maintain penile erection sufficient for conducting sexual intercourse [1]
Compounds acting via cyclic adenosine monophosphate, such as prostaglandin E1 (PGE1) and vasoactive intestinal polypeptide (VIP), are used in self-injection or topical regimens for the management of ED [9,10]
Combining Medicated Urethral System for Erection (MUSE) and sildenafil may be more efficacious in the salvage of patients who were in favor of non-invasive therapy when single-treatment modalities failed
Summary
Erectile dysfunction (ED) is defined as the consistent inability to attain or maintain penile erection sufficient for conducting sexual intercourse [1]. There is a high prevalence of ED in patients sharing risk factors known to contribute to the on-set of endothelial dysfunction, characterized by an impairment in the endothelium-dependent vasodilation triggered by NO (FMD = flow-mediated vasodilation brought about by sheer stress) [5,6,7]. Extensive coverage has been made on the NO/cyclic guanosine monophosphate (cGMP) pathway in penile erectile tissue [8]. This landmark discovery has enabled the development of drugs enhancing the intracellular levels of cyclic GMP, in particular, the phosphodiesterase (PDE) inhibitors sildenafil, tadalafil, vardenafil and avanafil. In human corpus cavernosum tissue, the intracellular level of cyclic AMP is under the control of the cyclic AMP-degrading PDE isoenzymes type 3 and 4 [11]
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