Abstract

The role of nitric oxide (NO) in erectile physiology is well documented. NO activates relaxation of corporal cavernosal smooth muscle tissue resulting in increased blood flow into the penis resulting in an erection. At present, pharmacologic treatments for erectile dysfunction, such as the phosphodiesterase-5 inhibitors, potentiate the erectile response generated by NO. However, a new class of treatments at a preclinical stage may allow localized delivery of NO to the penis via cutaneous application. These treatments may be of particular value to patients with a neurogenic component to their erectile dysfunction, and may act synergistically with phosphodiesterase-5 inhibitors to increase their efficacy.

Highlights

  • 20 Burnett AL, Musicki B, Jin L, Bivalacqua TJ

  • Oral phosphodiesterase-5 (PDE5) inhibitors are an effective treatment for erectile dysfunction (ED) in most patients

  • PDE5 inhibitors are ineffective for several subpopulations of patients, those with a neurogenic component underlying their ED

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Summary

Ion channels

Adenoviral vectors expressing several of the NOS isoforms (eNOS, nNOS, iNOS) when injected into the penis have been shown to increase both cGMP formation and erectile response in both aging and diabetic models of ED [15,16] Another approach has been adopted to use intracorporal injection of siRNA against the protein inhibitor of NOS (PIN). Studies demonstrated that application of nitroglycerin paste could result in a greater increase in penile circumference than a placebo, suggesting there was increased blood flow in the penis This did not correspond to an erection sufficient for satisfactory sexual performance, perhaps because effective local levels of NO were not reached, and there are no recent reports detailing the use of this compound in treating ED. The erections were typically of less than 2 min duration (average 1.42 min), which is the normal duration of erection in a rat

Argininosuccinate synthase
Conclusion
Executive summary
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