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Review |
From * The James Buchanan Brady Urological
Institute, Department of Urology, and the
Division of Cardiology, Department of
Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland.
| Correspondence to: Dr Trinity J Bivalacqua, The James Buchanan Brady Urological Institute, Johns Hopkins Medical Institutions, 600 N Wolfe Avenue, Marburg 143, Baltimore, MD 21287 (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, neurogenic dysfunction, or both.
The constitutive forms of nitric oxide synthase (NOS, endothelial [eNOS] and
neuronal [nNOS]) are important enzymes involved in the production of nitric
oxide (NO) and thus regulate penile vascular homeostasis. Given the effect 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 posttranslation modification in various vascular diseases of
the penis.
Key words: eNOS, nNOS, corpus cavernosum, phosphorylation
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