The anatomic mechanism of penile erection was discovered in the 1980s by electron microscopy of corrosion penile casts made in the flaccid state and during erection (_{Fournier et al, 1987; Banya et al, 1989}). In these models, the flaccid corpus cavernosum shows contracted sinusoids with constricted arteries and arterioles, and the draining venules form a plexus under the tunica albuginea. During erection, dilation of the arterial tree, expansion of the sinusoids, and compression of the subtunical and emissary veins are clearly seen. From these studies and observation of vasodilator-induced erections, it appears that the smooth muscles in the arterial tree and the trabeculae are the key to the erectile process.

The intrinsic smooth-muscle tone and, possibly, the adrenergic tonic discharge maintain contraction of the smooth muscles and the arterioles in the flaccid state. When the smooth muscles relax owing to release of neurotransmitters, the resistance to incoming flow drops to a minimum. This allows arterial and arteriolar vasodilatation and expansion of the sinusoids to receive a large increase of flow. Trapping of blood causes the penis to lengthen and widen rapidly until the capacity of the tunica albuginea is reached. Meanwhile, expansion of the sinusoidal walls against one another and against the tunica albuginea results in compression of the subtunical venular plexus. Meanwhile, uneven stretching of the layers of the tunica albuginea also compresses the emissary veins and effectively reduces the venous flow to a minimum (_{Lue, 2000;}

Figure 37-3A and B).