Dr. med. Dirk Manski



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Erection of the Penis: Anatomy and Physiology

References: (Benninghoff, 1993 ) (Porst, 2004).

Phases of the Penile Erection

Flaccid phase:

Low arterial and venous blood flow.

Filling phase of the erection:

the smooth muscle relaxation of the arteries leads to a drastic increase of 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.

Tumescence phase:

after reaching the submaximal volume of the erectile tissue the pressure rises in the corpora cavernosa to 80–90% of the systolic pressures. With increasing pressure, the emissary veins are compressed and the venous outflow is reduced. After reaching the systolic blood pressure a decrease of arterial flow and venous outflow is obtained.

Rigidity phase:

the contraction of Mm. bulbocavernosus and ischiocavernosi rises the pressure in the cavernous body up to several hundred mmHg. During this phase, there is no blood flow within the erectile tissues.

Detumescence phase:

a reduced arterial inflow leads to the reduction of pressure, this facilitates the venous outflow by the lack of compression of the emissary veins.

Neural Control of the Erection

Afferent neural pathway of erection:

infraspinal as well as supraspinal influences on the spinal erection center can trigger the erection (see innervation of the penis).

Reflexogenic erection:

a genital stimulation leads to a reflexogenic erection. Afferent signal pass via the pudendal nerve to the sacral erection center, this sends the efferent signal via the inferior hypogastric plexus. The reflexogenic erection is largely independent of cortical influences, as this kind of erection can remain intact after cervical or thoracic spinal cord injuries.

Psychogenic erection:

the cortical processing of sensory, visual, auditory stimuli or fantasies are triggers for 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 the psychogenic impotence is the existence of NPT, in contrast to serious vascular erectile dysfunction. Sympathetic centers mediate nocturnal erections, the existence of NPT still cannot rule out damage to the sacral parasympathetic erection center.

Efferent neuronal pathway of erection:

the stimulation of the autonomic nervous system, which influences the penile blood vessels, causes the 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. Location of the parasympathetic erection center: S2–4. Location of the sympathetic erection center: T12–L2. Starting from the spinal cord, the innervation passes 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 the rigidity phase of the erection.

Molecular Signaling of erection

Molecular mechanisms of erection:

the parasympathetic cavernous nerve activity leads to the release of NO (nitric oxide), a signal molecule which leads to the relaxation of 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, increase of cyclic GMP (cGMP), activation of protein kinases and phosphorylation of proteins and ion channels, 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.

Detumescence:

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 through the following intermediate steps also leads to the termination of the erection: stimulation of adrenergic receptors, phospholipase C, inositol triphosphate (IP3) and DAG (diacylglycerol), protein kinase C, intracellular calcium influx with smooth muscle contraction.







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



References anatomy of the penis

Benninghoff 1993 BENNINGHOFF, A.:
Makroskopische Anatomie, Embryologie und Histologie des Menschen.
15. Auflage.
München; Wien; Baltimore : Urban und Schwarzenberg, 1993

Porst 2004 PORST, H.:
Tadalafil, Therapiestrategien bei erektiler Dysfunktion.
Linkenheim-Hochstetten : Aesopus Verlag, 2004


  Deutsche Version: Erektion des Penis.