Abstract
INTRODUCTION AND OBJECTIVES: In addition to a loss of nitrergic function, cavernous nerve injury (CNI) in rats and radical prostatectomy in men result in an enhancement of adrenergic-neurogenic contractions of cavernosal tissue. Our aim was to evaluate the modulation of a-adrenergic system as a strategy to relieve erectile dysfunction (ED) and functional cavernosal alterations induced by CNI in rats. The effects of a-adrenergic blockade on neurogenic relaxation of human corpus cavernosum (HCC) were also evaluated. METHODS: Bilateral crush CNI (BCNI) was induced in anesthetized rats that were randomly selected to receive or not the non-selective a-blocker, phentolamine (1 mg/kg/day; PHENT) or the selective a1A-blocker, silodosine (0.1 mg/kg/day; SILOD) in drinking water for 4 weeks. Erectile responses to cavernosal nerve stimulation and neurogenic responses of corpus cavernosum to electrical field stimulation (EFS) in organ chambers were then evaluated. HCC from ED patients were obtained at the time of penile prosthesis implantation and nitrergic responses to EFS were determined. RESULTS: Chronic treatment with SILOD significantly improved erectile responses, partially recovered nitrergic relaxations and normalized neurogenic contractions (Table). Chronic a-blockade with PHENT or SILOD allowed for a significant potentiation of erectile responses in BCNI rats after acute administration of the PDE5 inhibitor tadalafil (0.3 mg/kg; i.v.). Treatment of HCC with PHENT (1 mM) slightly increased nitrergic relaxations and enhanced the potentiating effects of tadalafil (30 nM) on these responses. CONCLUSIONS: a-adrenergic modulation, especially selective a1A-blockade, improves erectile and cavernosal functions after BCNI. Modulation of adrenergic system, mainly in combination strategies, could have a role in the management of ED after RP.
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