The physiological role of testosterone in erectile function

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Abdulmaged M. Traish, PhD with N. Kim^1,2; R. Munarriz^1,2;, S. Jeong^1,2; I. Goldstein^1,2 ; 
¹Boston University School Of Medicine, Boston, USA; ²Institute For Sexual Medicine, Boston University School Of Medicine, Boston, USA

Penile erection is a haemodynamic process that depends on the structural and functional integrity of the erectile tissue. Increasingly, androgens are thought to play an important role in maintaining erectile function. We postulate that androgens dynamically and reversibly regulate the expression of paracrine growth factors that maintain the structural and functional integrity of the cellular components of erectile tissue. Using an animal model, we demonstrated a significant reduction in the erectile response to pelvic nerve stimulation after 2 or 4 weeks of androgen deprivation by surgical castration (orchiectomy). Similar changes were observed after 4 or 8 weeks of medical castration (LH-RH agonist).  Testosterone, but not oestradiol, reversed the effects of castration and restored erectile function to levels that were indistinguishable from intact animals. Castration also significantly reduced trabecular smooth muscle content relative to connective tissue and this reduction was reversed by testosterone but not by oestradiol treatment. Neural nitric oxide synthase protein expression and total activity was not altered significantly by castration or testosterone replacement in this animal model. However, phosphodiesterase type 5 activity increased in castrated animals treated with testosterone. Administration of Vardenafil (10 µg/kg), a PDE type 5 inhibitor, did not enhance erectile function in surgically orchiectomised or LH-RH agonist-treated animals. We also suggest that in the absence of androgen, erectile function is not restored by PDE type 5 inhibitors. We conclude that androgen insufficiency produces structural alterations in the corpus cavernosum smooth muscle and endothelium resulting in altered cellular signaling and corporal veno-occlusive dysfunction.