Erectile dysfunction is an extremely prevalent condition globally and has been estimated to increase dramatically over recent decades. Genetics or increased reporting alone cannot account for this phenomenon, and thus environmental factors have a likely role in the aetiology. As penis development relies on a delicate balance of endocrine signalling, exposure to endocrine-disrupting chemicals (EDCs) may alter patterning of the penis tissue to increase the risk of erectile dysfunction in adult life. Indeed, animal studies have confirmed that exposure to estrogenic-EDCs alters the structure of the corpus cavernosum (CC), a key vascular structure mediating erection via relaxation of the smooth muscle to increase blood flow into the penis.
However, there are currently very few developmental studies examining the links between estrogenic-EDC exposures and erectile dysfunction. Thus, I am exposing developing male mice to the potent estrogen diethylstilbestrol (DES) at a high and low dose which reflects environmentally relevant estrogen exposure. I subsequently rear the males to adulthood and dissect the CC to determine the impact of DES on smooth muscle action using wire myography. I hypothesise that individuals exposed to DES will display altered function of the CC, suggesting a predisposition to erectile dysfunction. This project will lead to a better understanding of the contribution of estrogenic-EDCs to erectile dysfunction, which is critical given the increasing global prevalence of this condition correlates with our exposure to EDCs.