Erection is a hemodynamic phenomenon involving the tissue of the corpora cavernosa as well as the corpus spongiosum in the penis. This tissue is a complex admixture of smooth muscle, endothelial cells, fibroblasts, and nerves interacting under stimulatory conditions to drastically enhance and maintain an accessory blood supply that imparts rigidity to the penis. Given the need for stringent control of blood flow during this response, it is no surprise that vascular insufficiency has the ability to drastically suppress erectile capability. In fact, penile vascular insufficiency is believed to be a very common pathomechanism of erectile dysfunction. This is associated with substantial pathologic changes in the erectile tissue leading to reduction in vascular smooth muscle cells and increases in collagen and fibrosis.
The currently available treatments of erectile dysfunction induce temporary erections at the time of administration of such treatments. However, these treatments do not address or cure the basic vascular/cavernosal pathology causing erectile dysfunction. The rationale for a curative treatment that improves or repairs the vascular structure and function of the erectile tissue is based upon an understanding of erectile physiology and the pathophysiology of vascular erectile dysfunction. Consequently, it is prudent to pursue investigation of factors that induce new vascular structure formation or vasculogenesis.