| Sexual Health |
The male erectile response is a vascular event initiated by neuronal action and maintained by a complex interplay between
vascular and neurological events. In its most common form, it is initiated by a central nervous system event that integrates
psychogenic stimuli (perception, desire, etc.) and controls the sympathetic and parasympathetic innervation of the penis.
Sensory stimuli from the penis are important in continuing this process and in initiating a reflex arc that may cause erection
under proper circumstances and may help to maintain erection during sexual activity.
Parasympathetic input allows erection by relaxation of trabecular smooth muscle and dilation of the helicine arteries of the
penis. This leads to expansion of the lacunar spaces and entrapment of blood by compressing venules against the tunica
albuginea, a process referred to as the corporal veno- occlusive mechanism. The tunica albuginea must have sufficient
stiffness to compress the venules penetrating it so that venous outflow is blocked and sufficient tumescence and rigidity can
occur.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second
nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the
endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this
nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other
potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the
trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic
guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
Constriction of the trabecular smooth muscle and helicine arteries induced by sympathetic innervation makes the penis
flaccid, with blood pressure in the cavernosal sinuses of the penis near venous pressure. Acetylcholine is thought to
decrease sympathetic tone. This may be important in a permissive sense for adequate trabecular smooth muscle relaxation
and consequent effective action of other mediators in achieving sufficient inflow of blood into the lacunar spaces. When the
trabecular smooth muscle relaxes and helicine arteries dilate in response to parasympathetic stimulation and decreased
sympathetic tone, increased blood flow fills the cavernous spaces, increasing the pressure within these spaces so that the
penis becomes erect. As the venules are compressed against the tunica albuginea, penile pressure approaches arterial
pressure, causing rigidity. Once this state is achieved, arterial inflow is reduced to a level that matches venous outflow.
vascular and neurological events. In its most common form, it is initiated by a central nervous system event that integrates
psychogenic stimuli (perception, desire, etc.) and controls the sympathetic and parasympathetic innervation of the penis.
Sensory stimuli from the penis are important in continuing this process and in initiating a reflex arc that may cause erection
under proper circumstances and may help to maintain erection during sexual activity.
Parasympathetic input allows erection by relaxation of trabecular smooth muscle and dilation of the helicine arteries of the
penis. This leads to expansion of the lacunar spaces and entrapment of blood by compressing venules against the tunica
albuginea, a process referred to as the corporal veno- occlusive mechanism. The tunica albuginea must have sufficient
stiffness to compress the venules penetrating it so that venous outflow is blocked and sufficient tumescence and rigidity can
occur.
Acetylcholine released by the parasympathetic nerves is thought to act primarily on endothelial cells to release a second
nonadrenergic-noncholinergic carrier of the signal that relaxes the trabecular smooth muscle. Nitric oxide released by the
endothelial cells, and possibly also of neural origin, is currently thought to be the leading of several candidates as this
nonadrenergic-noncholinergic transmitter; but this has not yet been conclusively demonstrated to the exclusion of other
potentially important substances (e.g., vasoactive intestinal polypeptide). The relaxing effect of nitric oxide on the
trabecular smooth muscle may be mediated through its stimulation of guanylate cyclase and the production of cyclic
guanosine monophosphate (cGMP), which would then function as a second messenger in this system.
Constriction of the trabecular smooth muscle and helicine arteries induced by sympathetic innervation makes the penis
flaccid, with blood pressure in the cavernosal sinuses of the penis near venous pressure. Acetylcholine is thought to
decrease sympathetic tone. This may be important in a permissive sense for adequate trabecular smooth muscle relaxation
and consequent effective action of other mediators in achieving sufficient inflow of blood into the lacunar spaces. When the
trabecular smooth muscle relaxes and helicine arteries dilate in response to parasympathetic stimulation and decreased
sympathetic tone, increased blood flow fills the cavernous spaces, increasing the pressure within these spaces so that the
penis becomes erect. As the venules are compressed against the tunica albuginea, penile pressure approaches arterial
pressure, causing rigidity. Once this state is achieved, arterial inflow is reduced to a level that matches venous outflow.
Physiology of erection
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