Journal of Andrology Testis Workshop 2009
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Published-Ahead-of-Print April 2, 2009, DOI:10.2164/jandrol.108.006999

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Post-Translational Modification of Constitutive Nitric Oxide Synthase in the Penis

Biljana Musicki , Ashley E Ross , Hunter C Champion , Arthur L. Burnett , and Trinity J Bivalacqua *

* To whom correspondence should be addressed. E-mail: tbivala1{at}jhmi.edu.

Erectile dysfunction (ED) is a common men's health problem characterized by the consistent inability to sustain an erection sufficient for sexual intercourse. Basic science research on erectile physiology has been devoted to investigating the pathogenesis of ED and has led to the conclusion that ED is predominately a disease of vascular origin and/or neurogenic dysfunction. The constitutive forms of nitric oxide synthase [NOS; endothelial NOS (eNOS) and neuronal NOS (nNOS)] are important enzymes involved in the production of nitric oxide (NO) and thus regulate penile vascular homeostasis. Given the impact of endothelial- and neuronal-derived NO in penile vascular biology, a great deal of research over the past decade has focused on the role of NO synthesis from the endothelium and nitrergic nerve terminal in normal erectile physiology as well as in disease states. Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in the occurrence of ED. Therefore, molecular mechanisms involved in dysregulation of these NOS isoforms in the development of ED are essential to discovering the pathogenesis of ED in various disease states. This communication reviews the role of eNOS and nNOS in erectile physiology and discusses the alterations in eNOS and nNOS via post-translation modification in various vascular diseases of the penis.


Key words: Erectile Dysfunction • Penis • endothelium • nitric oxide • nitric oxide synthase






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