Direct effects of testosterone on erection

Androgens and a functioning androgen receptor are necessary for normal development of the human penis. In humans, the penis grows in phases, initially during early gestation and then continuing until approximately the age of five. A latency period follows until puberty, when penile size responds to the increase of testosterone levels. Growth ceases at the completion of pubertal growth despite continued high levels of circulating testosterone. The exact mechanism of penile growth cessation remains unresolved, but is probably not only due to down regulation of androgen receptors (Baskin etal. 1997; Levy etal. 1996).

Numerous studies in animal models have demonstrated a direct testosterone-dependency of erection. In castrated rats, the intracavernosal blood pressure of the penis was insufficient in response to induced erection by electrical field stimulation of the cavernosal nerve. Testosterone replacement restored the normal erectile response (Mills etal. 1994). In the rat, the primary mode of action of testosterone for erectile function seems to be the stimulation of neurogenic and endothelial nitric oxide synthesis (e.g. Baba et al. 2000a; 2000b; Chamness et al. 1995; Garban et al. 1995;Marin etal. 1999; Park etal. 1999;Penson etal. 1996; Reilly etal. 1997;Schirar etal. 1997; Seftel 1997; Zvara etal. 1995). This effect is mediated by testosterone or dihydrotestosterone, but not by estradiol (Lugg etal. 1995). In addition, castration induces programmed smooth muscle cell death in the rat penis, indicating that androgens may have an important role in maintaining smooth muscle growth and functional integrity (Shabsigh 1997).

In a different species, the New Zealand white rabbit, castration similarly reduces intracavernosal blood pressure during stimulation of the cavernosal nerve for induced erection (Traish et al. 1999). Testosterone, but not estradiol treatment prevented the effects of castration and restored intracavernosal pressure to values comparable to those obtained in intact animals. Interestingly, no change of the neuronal nitric oxide synthase protein expression and total activity were observed after castration or testosterone replacement (Traish et al. 1999; 2003). However, testosterone deficiency induced by castration or administration of GnRH agonists reduced trabecular smooth muscle content, and this reduction was restored by testosterone, and not by estradiol (Traish et al. 2003). The imbalance between smooth muscle and extracellular matrix in testosterone deficiency can lead to veno-occlusive dysfunction of the penis, and thereby cause erectile dysfunction (Mills et al. 1998). Comparable results indicating an androgen-dependent mechanism of veno-occlusive erectile dysfunction have recently been described in a castrated mouse model (Palese etal. 2003).

In humans, dynamic colour duplex ultrasound after pharmaco-stimulation of erection indicates that in men with erectile dysfunction low free testosterone levels correlate independently of age with impaired relaxation of cavernous smooth muscle cells (Aversa etal. 2000). Other studies demonstrated a significant increase of testosterone concentration in blood samples taken from the corpus cavernosum in healthy males during the tumescence and rigidity phase of erection, whereas no significant change was detected in patients with organogenic erectile dysfunction (Becker etal. 2000; 2001).

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