Toxicology reports · 2025
Sildenafil effect on testosterone-induced prostate hypertrophy and relaxation of urinary bladder neck muscles.
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El-Dwairi Qasim A, Alzoubi Karem H, Mahafdeh Rania
Аннотация
BACKGROUND: Previous studies have demonstrated the expression of phosphodiesterase-5 receptors in prostate tissue. In this study, we investigated the efficacy of sildenafil citrate in testosterone-induced benign prostate hyperplasia (BPH) in rabbits.
METHODS: Prostate hyperplasia was induced using testosterone propionate for 8 weeks. Rabbits were divided into two groups: control and experimental. The experimental group was further subdivided into two subgroups: one subgroup was sacrificed after testosterone induction, while the other subgroup received sildenafil (5 mg/kg/day) via intragastric intubation for 8 weeks. The weight of the prostate and relaxation of the bladder neck muscle were assessed. Organ bath experiments evaluated the effect of sildenafil on phenylephrine-precontracted bladder neck muscle strips.
RESULTS: The mean prostate weight was reduced by 65.34 % after 8 weeks of treatment with sildenafil in animals with BPH. Sildenafil induced significant smooth muscle relaxation of the phenylephrine-contracted bladder neck muscle strips. The mean relaxation value was 2.11 ± 0.13, representing a 32.8 % reduction in contraction percentage. Maximal relaxation was produced at 5.0 × 10⁻⁶ M of sildenafil. Sildenafil induced significant relaxation of the phenylephrine-contracted bladder neck muscle strips. Adding the nitric oxide synthase inhibitor L-NAME inhibited relaxation, whereas sodium nitroprusside, a nitric oxide donor, increased it. Histopathological analysis showed increased papillary projections, acinar areas, and epithelial thickness in the testosterone-treated group. Sildenafil treatment reversed the hypertrophic and hyperplastic changes.
CONCLUSIONS: The results indicate that sildenafil may provide a dual function in the treatment of erectile dysfunction and the relief of urinary tract complications associated with prostatic hypertrophy.
METHODS: Prostate hyperplasia was induced using testosterone propionate for 8 weeks. Rabbits were divided into two groups: control and experimental. The experimental group was further subdivided into two subgroups: one subgroup was sacrificed after testosterone induction, while the other subgroup received sildenafil (5 mg/kg/day) via intragastric intubation for 8 weeks. The weight of the prostate and relaxation of the bladder neck muscle were assessed. Organ bath experiments evaluated the effect of sildenafil on phenylephrine-precontracted bladder neck muscle strips.
RESULTS: The mean prostate weight was reduced by 65.34 % after 8 weeks of treatment with sildenafil in animals with BPH. Sildenafil induced significant smooth muscle relaxation of the phenylephrine-contracted bladder neck muscle strips. The mean relaxation value was 2.11 ± 0.13, representing a 32.8 % reduction in contraction percentage. Maximal relaxation was produced at 5.0 × 10⁻⁶ M of sildenafil. Sildenafil induced significant relaxation of the phenylephrine-contracted bladder neck muscle strips. Adding the nitric oxide synthase inhibitor L-NAME inhibited relaxation, whereas sodium nitroprusside, a nitric oxide donor, increased it. Histopathological analysis showed increased papillary projections, acinar areas, and epithelial thickness in the testosterone-treated group. Sildenafil treatment reversed the hypertrophic and hyperplastic changes.
CONCLUSIONS: The results indicate that sildenafil may provide a dual function in the treatment of erectile dysfunction and the relief of urinary tract complications associated with prostatic hypertrophy.