Objective: Our earlier studies showed that endogenous hydrogen sulfide (H(2)S) pathway contributed significantly to erectile function. In this study, we tested the hypothesis that age-dependent changes in the bioavailability of H(2)S increased the risk of erectile dysfunction (ED).
Methods: Young, adult (3-month) and older (18-month) male Sprague-Dawley rats (n = 6-8/group) were treated daily with sodium hydrosulfide hydrate (NaHS), DL-propargylglycine, sildenafil or l-NAME for 10 weeks. Subsequent to cavernous nerve electrical stimulation, intracavernosal pressure (ICP) responses were determined, and the samples were collected and processed for hormonal (plasma) and gaseous parameters (plasma and erectile corpus cavernosum [CC]) using standard assay protocols.
Results: Aging significantly reduced the ICP response (35.9 ± 2.0 mmHg vs. 45.2 ± 1.9 mmHg in young controls), which was countered by NaHS (53.5 ± 6.0) or sildenafil (52.8 ± 9.8) treatment. In these rats, marked increments to testosterone (T) or estradiol resulted from NaHS supplementation. Similar to age-dependent decline in NO, the plasma and CC level of H(2)S was significantly lower in senescent rats when compared with young animals (p < 0.05).
Conclusion: Our results confirm that ED with aging may be linked to a derangement in the H(2)S pathway accompanied by low T levels. It is likely that a pharmacologic intervention delivering H(2)S will provide additional benefits to sexual function from an improved T milieu.