ABSTRACT
Major scientific advances have occurred in the study of erection physiology at the molecular level. Specific signaling pathways have been described that provide a molecular biologic basis for penile erection. Our current understanding is that penile erection is mainly mediated by the nitric oxide (NO) pathway. 3,4 NO is synthesized by neuronal nitric oxide synthase (nNOS), expressed in autonomic nerve endings, and by endothelial nitric oxide synthase (eNOS), expressed in vascular and sinusoidal endothelium of the penis. Neuronally derived NO initiates penile erection, while endo thelial NO maintains erection. 5 Accordingly, the common factors contributing to ED include reduced activity of nNOS and eNOS and decreased NO bioavailability ( Figure 10.2 ). cGMP and cAMP are primary intracellular mediators of corporal smooth muscle relaxation. 3,4 Opposing this activity, the RhoA – Rhokinase signaling pathway is the main mediator of cavernosal tissue contraction. 6-8 Derangements of these mechanisms probably explain the pathophysiology of ED associated with different disease states.
