title: Posttranslational modification of constitutive nitric oxide synthase in the penis.
abstract: 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.
authors.affiliation: The James Buchanan Brady Urological Institute, Department of Urology, Johns Hopkins Medical Institutions, 600 N Wolfe Avenue, Marburg 143, Baltimore, MD 21287, USA.
authors.forename: Biljana
authors.initials: B
authors.lastname: Musicki
authors.forename: Ashley E
authors.initials: AE
authors.lastname: Ross
authors.forename: Hunter C
authors.initials: HC
authors.lastname: Champion
authors.forename: Arthur L
authors.initials: AL
authors.lastname: Burnett
authors.forename: Trinity J
authors.initials: TJ
authors.lastname: Bivalacqua