E RECTION is a complex hemodynamic event regulated by the tone of smooth muscle composing the cavernous arterioles, venules, and sinusoids. In the flaccid penis baseline ot-adrenergic stimulation maintains the smooth muscle of the cavernous arterioles and corporal sinusoids contracted. Although vascular resistance to inflow is elevated in the flaccid state, venular outflow is unrestricted. Regulation of venous outflow from the penis appears to be a passive phenomenon; venules draining the sinusoidal spaces coallesce into a plexus below the outer fibroelastic tunica of the paired corporal bodies. Egress from the subtunical venular plexus is via emissary veins exiting perpendicularly through the tunica albuginea into the deep dorsal vein or directly via the cavernous and crural veins at the base of the corporal bodies. 1 Erection is initiated by at least three welldocumented neuropharmacologic stimulants2-5: 1. Inhibition or decrease in excitation of postsynaptic or-1 receptors on cavernous and arteriolar muscle. 2. Increasing cholinergic transmission: Acetylcholine acting on postganglionic adrenergic fibers inhibits norepinephrine release. Acetylcholine mediates the release of endothelial relaxant factor, which rapidly diffuses to the smooth muscle of arteriolar walls. 3. Direct nonadrenergic noncholinergic (NANC) transmission: Several substances have previously been considered to be the NANC erection transmitter (vasoactive intestinal peptide, substance P, prostaglandin E, adenosine triphosphate). Nitric oxide is currently believed to be the principal regulator of NANC corporal relaxation; penile smooth muscle relaxation is initiated by intracellular accumulation of cyclic guanosine monophosphate (cGMP). Tumescence follows a decrease in corporal smooth muscle tone and vascular resistance; arterial inflow increases and the corpora sinusoids distend with oxygenated blood. The expanding sinusoids compress the subtunical plexus and restrict venous outflow. Approximately 90% of systemic arterial pressure is transmitted to the corporal bodies as a result of increased arterial inflow and veno-occlusion. Observations of pudendal and cavernous arterial inflows and intracorporal pressures in the animal model reveal that erection can be divided into six phases: flaccid, latent, tumescence, full erection, rigid erection, and detumescence. 6 Figure 1 shows that cavernous nerve stimulation produces erection with intracorporal pressure reaching 100 mmHg during full erection and transiently exceeding 100 mmHg during the rigid phase. Contemporary clinical studies using intracavernous agents (papaverine, phentolamine, prostaglandin El, and vasoactive intestinal peptide) have revealed that impotence is most often organic in origin and predominantly vasculogenic in etiology 7-11 We believe that color duplex Doppler ultrasound (CDDU) following intracorporal vasoactive stimulation is the most reliable and least invasive means of screening for vasculogenic erectile failure and for selecting patients for more invasive tests of pathologic corporal inflow or outflow. The principles, techniques, and most recent criteria for duplex Doppler penile blood flow are reviewed.