We propose that extensive morphological changes in penile smooth muscle and endothelium observed postprostatectomy in the corpora cavernosa are a major contributing factor to ED development. Interventions targeted to prevent cavernous nerve (CN)-induced apoptosis in the penis would be a powerful tool to prevent postprostatectomy ED.
The process of erection is complex, involving critical integration of vascular, neural, hormonal, and morphological influences. As ED develops, the balance between these processes becomes skewed. In both diabetic and CN injury ED models, there is a general impairment in responsiveness of the rat corpora cavernosa, impaired smooth muscle relaxation, a significant decrease in abundance of the smooth muscle and endothelium of the corpora cavernosa, and an increase in the ratio of apoptotic cells in the erectile tissue. Current treatments for ED aim to increase smooth muscle relaxation. However, as the smooth muscle morphology of the corpora cavernosa becomes increasingly abnormal following prostatectomy, these traditional treatment strategies become less effective and eventually fail. In these studies we propose a novel approach, in which we aim to elucidate the underlying mechanisms that cause apoptosis of the corpora cavernosal smooth muscle, and thus cause ED to occur.