Journal of Andrology
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Published-Ahead-of-Print July 17, 2008, DOI:10.2164/jandrol.107.004630

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Testosterone and Erectile Dysfunction

Aksam A. Yassin * and Farid Saad

* To whom correspondence should be addressed. E-mail: yassin{at}t-online.de.

Erectile dysfunction (ED) is defined as the inability to achieve or maintain erections sufficient for satisfactory sexual intercourse. Formerly dismissed as a psychological condition, ED is now known as a treatable disorder and an important risk-marker for cardiovascular disease. The physiological mechanism of normal penile erection is dependent on trapping incoming blood within the cavernosal bodies to increase pressure and volume. This physiological process, namely the veno-occlusive mechanism, depends upon the integrity of endocrine, hormonal, neurological and vascular components, as well as the fibroelastic properties of the cavernosal tissue. The penile corpus cavernosum is a vascular bed, and any alterations to its structure can produce vascular dysfunction. Cavernosal tissues from men with erectile dysfunction have been demonstrated to exhibit reduced lacunar spaces, reduced smooth muscle content, and a concomitant increase in connective tissue deposition. Indeed, changes in penile tissue structural integrity is thought to contribute to veno-occlusive dysfunction. Recent research has identified a number of the key mediators of normal erectile function, with nitric oxide (NO) being one of the most important. However, many of the pathophysiological mechanisms of ED remain to be determined. It has been estimated that approximately 70% of ED is of organic origin, with the major risk factors being diabetes mellitus, hypercholesterolemia, smoking and chronic medical illnesses. These are also established risk factors for atherosclerosis, which is the predominant predisposing factor of vasculogenic ED.


Key words: Erectile Dysfunction • Penis • PDE-5 inhibitors • Testosterone




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