Pathophysiology of erectile dysfunction

Physiology of erection and pathophysiology erectile dysfunction is reviewed . Analysis is obtained from basic and clinical research including animals s tudies, anatomical studies, and molecular and cellular research on corporal tissue obtained during penile prosthesis implantation. Supraspinal influen ces and spinal influence on penile erection has been learned from spinal co rd injury patient. Corporal smooth muscle relaxation of penile arteries and corpus cavernosum leads to penile erection, results from parasympathetic/nonadrenergic noncho linergic neural pathway activation and simultaneous inhibition of sympathet ic outflow. Anatomical studies taught understanding of the mechanism for re striction of blood outflow from the corpora cavernosa. The change of smooth muscle tone has emerged as a key factor in erection and detumescence. Many independent factors converge on the modulation of corporal smooth muscle t one. Neuronal and local neurotransmitter effects via gap junction, potassiu m channels, and calcium channel. A nitric oxide/cyclic guanosine monophosph ate mechanism as well as cyclic aminomonophosphate has an important role in mediating the corporal smooth muscle relaxation necessary for erectile fun ction. Erectile dysfunction can be due to vasculogenic, neurogenic, hormona l, veno-occlusive, psychogenic and/or pharmacogenic factors as well as alte rations in the nitric oxide/cyclic guanosine monophosphate (cGMP) or cyclic aminophosphate (cAMP) pathway or other regulatory mechanisms including gap junction or ionic channel resulting in an imbalance in corporal smooth mus cle contraction and relaxation. Our present knowledge of the hemodynamics, functional anatomy, neurophysiol ogy, and neuropharmacology of penile erection and dysfunction at the cellul ar and molecular level has led to better understanding of physiology and pa thophysiology of erectile dysfunction.