The Neurophysiology of an Erection

When the NANC system is stimulated, nitrogen oxide (NO) is released within the smooth muscle cells of the penis. The NO is converted from L-Arginine by nitrogen oxide synthase, which in turn increases the production of cyclic guanosine monophosphate (cGMP). cGMP decreases the intracellular concentration of the calcium ions (Ca2+) that are essential for muscle contraction. In this case, the Ca2+ is decreased and smooth muscle relaxes, allowing blood flow to the penis causing expansion.

cGMP is broken down by phosphodiesterase type 5 (PDE5). When this occurs the Ca2+ increases in concentration in the cell, resulting in contraction of the smooth muscle cells and detumescence. Sildenafil ('Viagra') is a PDE5 inhibitor, and allows for erections to be maintained in response to stumuli. Although in itself, It will not initiate an erection.

When the sympathetic fibres are stimulated, noradrenaline (NA) is released from the nerve terminal. This activates alpha-1-adrenergic receptors to produce contraction of the smooth muscle of both the vasculature and the corpora cavernosum. This causes detumescence of the penis.