082 Testosterone Replacement Therapy may Upregulate Pro-erectile Markers by Modulating Endothelial Function In Hypogonadal Men with Erectile Dysfunction

Testosterone (T) deficiency (hypogonadism) is strongly associated with erectile dysfunction (ED). The relaxant response of T on non-genomic pathways on the corporal smooth muscle has been reported. However, there is no evidence on the in vitro mediating effects of T on human corpus cavernosum (HCC). We aimed to compare the mediating effects of different T concentrations on nitric oxide (NO)-dependent & -independent nitrergic relaxations in organ bath studies. HCC samples were obtained after consent from men undergoing penile prosthesis implantation (n = 9). After phenylephrine (Phe) contraction, electrical field stimulation (EFS), acetylcholine (ACh) and phosphodiesterase-5 (PDE-5) inhibitor (sildenafil) induced relaxation at 150, 400, and 600 ng/dL T incubations of HCC strips were performed using organ bath preparations. HCC measurements of endothelial nitric oxide synthase (eNOS), neuronal (nNOS) and PDE5 were evaluated through immunostaining, Western blotting, and cGMP and nitrite/nitrate assays. The relaxation responses to ACh and EFS in isolated HCC were significantly increased by all T levels, as compared to untreated tissues. However, sildenafil-induced relaxant responses were significantly increased at eugonadal T. The unaltered neurogenic contractions to EFS were observed. Eugonadal T levels may be accompanied by increased eNOS, nNOS and cGMP, along with lower PDE5 protein expressions. Tissue nitrate/nitrite concentration (NO production marker) was enhanced by eugonadal T levels (see Table).