Chapter 17
is fl accid. During sexual excitation, the small arteries dilate,
blood fl ow increases, the three vascular compartments become
engorged with blood at high pressure, and the penis becomes
rigid (
). The vascular dilation is initiated by neural
input to the small arteries of the penis. As the vascular com-
partments expand, the veins emptying them are passively com-
pressed, furthur increasing the local pressure, thus contributing
to the engorgement while blood fl ow remains elevated. This
entire process occurs rapidly with complete erection sometimes
taking only 5 to 10 s.
What are the neural inputs to the small arteries of the
penis? At rest, the dominant input is from sympathetic neu-
rons that release norepinephrine, which causes the arterial
smooth muscle to contract. During erection this sympathetic
input is inhibited. Much more important is the activation of
nonadrenergic, noncholinergic autonomic neurons to the
arteries (
Figure 17–10
). These neurons and associated endo-
thelial cells release
nitric oxide,
which relaxes the arterial
smooth muscle.
Which receptors and afferent pathways initiate these
refl exes? The primary stimulus comes from mechano-receptors
in the genital region, particularly in the head of the penis. The
afferent fi bers carrying the impulses synapse in the lower spi-
nal cord on interneurons that control the efferent outfl ow.
It must be stressed, however, that higher brain centers,
via descending pathways, may also exert profound stimulatory
or inhibitory effects upon the autonomic neurons to the small
arteries of the penis. Thus, mechanical stimuli from areas
other than the penis, as well as thoughts, emotions, sights,
and odors, can induce erection in the complete absence of
penile stimulation (or prevent erection even though stimula-
tion is present).
Erectile dysfunction
(also termed impotence) is the
consistent inability to achieve or sustain an erection of suffi -
cient rigidity for sexual intercourse, and is a common problem.
Although it can be mild to moderate in degree, complete erec-
tile dysfunction is present in as many as 10 percent of adult
American males between the ages of 40 and 70. During this
period of life, its rate almost doubles. The organic causes are
multiple and include damage to or malfunction of the efferent
nerves or descending pathways, endocrine disorders, various
therapeutic and “recreational” drugs (e.g., alcohol), and certain
diseases, particularly diabetes mellitus. Erectile dysfunction
can also be due to psychological factors (such as depression),
which are mediated by the brain and the descending pathways.
There are now a group of orally active
type 5
including sildenafi l (
), var-
denafi l (
), and tadalafi l (
) that greatly improve
the ability of many men with erectile dysfunction to achieve
and maintain an erection. The most important event leading
to erection is the dilation of penile arteries by nitric oxide,
released from autonomic neurons. Nitric oxide stimulates the
enzyme guanylyl cyclase, which catalyzes the formation of
cyclic GMP, as described in Chapter 5. This second messen-
ger then continues the signal transduction pathway leading to
the relaxation of the arterial smooth muscle. The sequence of
events is terminated by an enzyme-dependent breakdown of
cGMP. PDE5 inhibitors block the action of this enzyme and
thereby permit a higher concentration of cGMP to exist.
The discharge of semen from the penis, called
primarily a spinal refl
ex mediated by afferent pathways from
penile mechanoreceptors. When the level of stimulation is high
enough, a patterned sequence of discharge of the efferent
neurons ensues. This sequence can be divided into two
phases: (1) the smooth muscles of the epididymis, vas defer-
ens, ejaculatory ducts, prostate, and seminal vesicles contract as a
result of sympathetic nerve stimulation, emptying the sperm and
glandular secretions into the urethra (
); and (2) the
semen, with an average volume of 3 ml and containing 300 mil-
lion sperm, is then expelled from the urethra by a series of rapid
contractions of the urethral smooth muscle as well as the skeletal
muscle at the base of the penis. During ejaculation, the sphincter
at the base of the urinary bladder is closed so that sperm cannot
enter the bladder, nor can urine be expelled from it. Note that
erection involves inhibition of sympathetic nerves (to the small
arteries of the penis), while ejaculation involves stimulation of
sympathetic nerves (to the smooth muscles of the duct system).
The rhythmical muscular contractions that occur during
ejaculation are associated with intense pleasure and many sys-
temic physiological changes, collectively termed an
Marked skeletal muscle contractions occur throughout the body,
and there is a transient increase in heart rate and blood pressure.
Once ejaculation has occurred, there is a latent period
during which a second erection is not possible. The latent
period is quite variable but may last from minutes to hours.
As is true of erectile dysfunction,
premature ejacula-
or failure to ejaculate can be the result of infl uence by
higher brain centers.
Neurons to penis
Activity of neurons that release nitric oxide
Activity of sympathetic neurons
Compression of veins
Descending CNS
pathways triggered by
thoughts, emotions, and
sensory inputs such as
sight and smell
Input from penis
Dilation of arteries
Figure 17–10
Refl ex pathways for erection. Nitric oxide, a vasodilator, is the most
important neurotransmitter to the arteries in this refl ex.
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