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MINIREVIEW

eNOS Function and Dysfunction in the Penis

Department of Urology, the Johns Hopkins Hospital, Baltimore, Maryland 21287

To whom requests for reprints should be addressed at ¹ Johns Hopkins Hospital, Department of Urology, Marburg 407, 600 North Wolfe Street, Baltimore, MD 21287. E-mail: aburnett{at}jhmi.edu

Endothelial nitric oxide (NO) synthase (eNOS) has an indispensable role in the erectile response. In the penis, eNOS activity and endothelial NO bioavailability are regulated by multiple post-translational molecular mechanisms, such as eNOS phosphorylation, eNOS interaction with regulatory proteins and contractile pathways, and actions of reactive oxygen species (ROS). These mechanisms regulate eNOS-mediated responses under physiologic circumstances and provide various mechanisms whereby endothelial NO availability may be altered in states of vasculogenic erectile dysfunction (ED). In view of the recent advances in the field of eNOS function in the penis and its role in penile erection, the emphasis in this review is placed on the mechanisms regulating eNOS activity and its interaction with the RhoA/Rho-kinase pathway in the physiology of penile erection and the pathophysiology of ED.

Key Words: eNOS • phosphorylation • Hsp90 • caveolin-1 • RhoA/Rho-kinase • reactive oxygen species • aging • diabetes • hypercholesterolemia • hypertension

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