2007/11/15 by Kazem M. Azadzoi, Mike B. Siroky · 1 citation
Medicine · Psychology · #Sexual function and dysfunction studies #Urinary Bladder and Prostate Research #Sexuality, Behavior, and Technology
paper · doi:10.1007/978-1-59745-155-0_9
openalex publication_date 2007/11/15 · openalex created_date 2025/10/10 · openalex updated_date 2026/08/04
The penis is innervated by parasympathetic nerves arising from the second to fourth sacral cord segments (pelvic nerves) that ultimately become the cavernosal nerves. Sympathetic innervation, via the hypogastric nerve and pelvic plexus, causes detumescence but may also serve as an alternate erectile pathway. Somatic (sensory and motor) nerves reach the penis via the pudendal nerve. In the female, the genital organs have a complex innervation that is not well understood. The pelvic nerves appear to subserve sensation from the vagina while the pudendal nerve subserves sensation from the labia and clitoris. In the male central nervous system, the medial dorsal nucleus of the thalamus and the medial pre-optic area are important centers that control penile erection and sexual drive. Serotonin tends to inhibit penile erection at both spinal and supraspinal sites while dopamine and dopamine agonists such as apomorphine tend to induce penile erection. Oxytocin appears to be an important facilitator of erection at the spinal and supraspinal levels. Nitric oxide (NO) has recently been added to the list of compounds that act in the central nervous system to facilitate penile erection. Peripheral control of erection is mediated through NO, which modulates cavernosal smooth muscle relaxation and vasodilation. Norepinephrine is the primary adrenergic transmitter in the penis and controls penile detumescence by inducing penile smooth muscle contraction. Acetylcholine has a variety of effects that tend to promote erection including co-release of NO and perhaps vasoactive intestinal polypeptide from cholinergic nerve terminals, release of NO from the vascular endothelium, and suppression of norepinephrine release. The mechanism of vaginal engorgement during sexual arousal involves vasodilation and significant changes in vaginal tone, including relaxation and lengthening. The clitoral and penile smooth muscle appears to share a similar neuroregulatory mechanisms.