The physiology of penile erection involves an interplay of anatomical, hemodynamic, neurophysiological, and sex hormone interaction. Penile erection is the result of a complex interaction between the central nervous system and other local factors. This physical event also can be influenced by psychological factors.
The penis is mainly supplied by the internal puden-dal artery, and three major sets of veins, superficial, intermediate, and deep veins, drain it. Drug-induced changes in neurotransmitter action can affect local blood flow. Vascular supply, intrinsic smooth muscles of the penis, and adjacent striated muscles are controlled by nerves arising from the thoracolumbar sympathetic, the lumbosacral parasympathetic, and the lumbosacral somatic systems. The pudendal nerve is the major somatic pathway innervating the male genitalia.
In addition to the integrated participation of the peripheral nerves, central neural pathways are involved in the process. These central mechanisms interact during normal sexual activity and require complex coordination between the autonomic nervous system and the somatic outflow at the level of the spinal cord.
5-Hydroxytryptamine (5-HT), dopamine, and nor-epinephrine play important roles as central neurotrans-mitters in the process of erection. Still other substances or hormones, such as endorphins, oxytocin, vasopressin, adrenocorticotropic hormone (ACTH) and related peptides, and prolactin, appear to participate in the complex and coordinated process of penile erection. Central nonadrenergic neurons also may influence male sexual behavior.
Nitric oxide (NO) released during nonadrenergic, noncholinergic (NANC) neurotransmission and from the vascular endothelium is most likely the major neu-rotransmitter mediating penile erection. NO is a mediator of relaxation of the corpus cavernosum in response to NANC neurotransmission. An endothelium-derived relaxing factor (EDRF) in the peripheral vasculature also can induce relaxation of vascular smooth muscles. NO functions as EDRF in many blood vessels, and its release from the endothelial cell relaxes vascular smooth muscle by activating soluble guanylate cyclase, thereby increasing the production of the intracellular messenger cGMP.
The role of NO in the physiology of male sexual function establishes its importance as the principal modulator of penile erection. An increase in cGMP activates specific protein kinases, which in turn phospho-rylate certain proteins, activate ion channels, and through intermediary biochemical events lead to reduction in cytosolic calcium and relaxation of smooth muscles. Following an erection or the return to a flaccid state, cGMP is hydrolyzed to GMP by phosphodi-esterase type 5 (PD-5). Although other types of phos-phodiesterases are present in the corpus cavernosum, they do not appear to play a significant physiological role in erection.
Certain drugs (e.g., sildenafil, vardenafil, and cialis) exert their pharmacological actions by inhibiting the breakdown of cGMP. Sildenafil (Viagra) is a selective inhibitor of PD-5, an enzyme that inactivates cGMP. Vardenifil (Levitra) is a particularly effective inhibitor of PD-5. It has a shorter onset of action and can be used in smaller doses than sildenafil. Other drugs used in the treatment of ED exert their effects through other biochemical pathways, both central and peripheral.
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