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Penile Erection: Physiology, Nervous System and Signal Transduction
- Anatomy of the Penis: gross appearance, vascular supply, histology.
- Anatomy of the Penis: phases of erection, innervation, neural control, molecular signaling.
Innervation of the Penis
The processing of sensory stimuli in the limbic system and hypothalamus stimulates the spinal autonomic centers of the erection. The main centers in the hypothalamus are the paraventricular nucleus and the medial area praeoptica. The neurotransmitters of these first neurons are Oxytocin, melanocortin, and dopamine.
Spinal Autonomic Centers:
Cortical and peripheral stimuli activate spinal centers and cause an erection. The Nucleus intermediolateralis (S2–S4) is the parasympathetic spinal center, and the sympathetic spinal center is located at Th12–L2.
Inferior hypogastric plexus:
Above mentioned centers send nerve fibers to the inferior hypogastric plexus, which are passed on to the pelvic organs.
Cavernous nerves of the penis:
The cavernous nerves of the penis consist of autonomic nerve fibers from the inferior hypogastric plexus. The nerve passes posterolateral to the seminal vesicles and lateral to the prostate (mainly located between 5 to 7 o'clock) to the penis. In the membranous portion of the urethra, the nerve fibers are located between 3 and 9 o'clock. At the distal bulb of the penis, they are located between 1 and 11 o'clock, where they enter the penis. In addition, nerve fibers accompany the arteries or sensory nerves. The autonomic nerve fibers innervate the helicine arteries. The cholinergic nerve endings stimulate the NO-synthase and, therefore, release NO (nitric oxide). The exact mechanism is explained below.
Motor neuron innervation:
The pudendal nerve (S2–4) innervates the bulbospongious and ischiocavernosus muscle.
Afferent nerve fibers run from the receptors via the dorsal penile nerve and pudendal nerve into the spinal cord. The following steps are either the medial lemniscus or the spinothalamic tract.
Phases of the Penile Erection
No erection, low arterial and venous penile blood flow.
Filling phase of the erection:
The smooth muscle relaxation of the arteries leads to a drastic increase in penile blood flow while the venous drainage remains constant. The volume of the penis increases and the filling is facilitated by the smooth muscle relaxation of the erectile tissue.
After reaching the submaximal volume of the erectile tissue, the pressure rises in the corpora cavernosa to 80–90% of the systolic pressure. With increasing pressure, the emissary veins are compressed and the venous outflow is reduced. Arterial flow and venous outflow decrease if the intracavernosal pressure reaches the systolic blood pressure.
The bulbospongiosus and ischiocavernosal muscles' contraction increases the intracavernosal pressure up to several hundred mmHg. During this phase, there is no blood flow within the erectile tissues.
A reduced arterial inflow reduces pressure, which facilitates the venous outflow by the lack of compression of the emissary veins.
Neural Control of the Erection
Afferent neural pathway of erection:
Infraspinal and supraspinal influences on the spinal erection center can trigger the erection (see innervation of the penis).
Genital stimulation leads to a reflexogenic erection. Afferent signals pass via the pudendal nerve to the sacral erection center, and efferent signals reach via the inferior hypogastric plexus the erectile tissue. The reflexogenic erection is mainly independent of cortical influences, as this kind of erection can remain intact after cervical or thoracic spinal cord injuries.
The cortical processing of sensory, visual, auditory stimuli or fantasies may trigger an erection. The cortical centers influence the sacral erection centers, which cause the erection via activation of the inferior hypogastric plexus.
Nocturnal erection occurs during the REM sleeping phase and can be measured during sleeping studies (Nocturnal penile tumescence = NPT). Typical for psychogenic impotence is the existence of NPT, in contrast to relevant vascular erectile dysfunction. Sympathetic centers mediate nocturnal erections, the presence of NPT still cannot rule out damage to the sacral parasympathetic erection center.
Efferent neuronal pathway of erection:
The autonomic nervous system controls the penile blood vessels and causes erection. The parasympathetic nervous system is pro-erectile; the sympathetic nervous system is anti-erectile (except for the nocturnal erection, see above).
The spinal cord contains the preganglionic neurons that innervate the penile vessels. S2–4 is the location of the parasympathetic erection center, and Th12–L2 is the location of the sympathetic erection center. The efferent neurons pass through the inferior hypogastric plexus via the cavernous nerves to the erectile tissue. The pudendal nerve from the sacral plexus innervates the pelvic floor muscles, whose contraction leads to the rigidity phase of the erection.
Molecular Signaling of Penile Erection
Molecular mechanisms of erection:
The parasympathetic cavernous nerve activity leads to the release of NO (nitric oxide), a signal molecule that relaxes the smooth muscles from the penile arterioles and erectile tissue.
Between the NO release and smooth muscle relaxation the following intermediate steps are necessary: activation of guanylyl cyclase with an increase of cyclic GMP (cGMP), activation of protein kinases and phosphorylation of proteins and ion channels, the opening of potassium channels and hyperpolarization of smooth muscle cells, lowering the intracellular concentration of calcium, missing activation of the muscle filaments (actin and myosin) and thus smooth muscle relaxation.
A decreasing parasympathetic innervation leads to the predominance of phosphodiesterase type 5, which interrupts the signal transduction cascade. The concentration of cGMP decreases, and the smooth muscle cells contract.
Adrenergic stimulation of the penis terminates erection through the following intermediate steps: stimulation of adrenergic receptors, phospholipase C, inositol triphosphate (IP3) and DAG (diacylglycerol), protein kinase C, intracellular calcium influx with smooth muscle contraction.
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Index: 1–9 A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Benninghoff 1993 BENNINGHOFF, A.:
Makroskopische Anatomie, Embryologie und Histologie des
München; Wien; Baltimore : Urban und Schwarzenberg, 1993
Porst 2004 PORST, H.:
Tadalafil, Therapiestrategien bei erektiler Dysfunktion.
Linkenheim-Hochstetten : Aesopus Verlag, 2004
Deutsche Version: Physiologie und Nervensteuerung der Erektion des Penis.