Male Reproductive Physiology
An erection is a complex
neuropsychologic event. It occurs when blood rapidly flows into the penis and
becomes trapped in its spongy chambers. The three systems directly involved in
a penile erection are: (i) the spongy corpora
cavernosa; (ii) the autonomic innervation of the penis; and (iii) the blood
supply of the penis. Sensory, peripheral and central nervous system pathways
integrate the response.
Although there are three erectile
bodies within the penis, the two corpora cavernosa are primarily responsible
for penile rigidity during an erection. The corpus spongiosum becomes tumescent
during an erection, but does not become rigid. It serves to redistribute the
intraurethral pressure so that the urethra remains patent and an effective
conduit for the ejaculate.
The basic physiology of an
erection is best understood if one considers each corpus cavernosum as if it
were a single lacunar chamber (Fig.
13.1a). Small (helicine) arteries transmit blood into the lacunar space, which
is bounded by smooth muscle within the trabecular wall. These arteries have
rigid, muscular walls. Exiting from the lacunar space are small venules that
coalesce into larger (subtunical) venules. The subtunical venules drain through
the tunica albuginea and form the emissary veins. Unlike arteries, veins have
very flexible walls and are readily compressed.
When the penis is flaccid, the
smooth muscle in the lacunar walls is in a contracted state. This contracted state
is maintained by noradrenergic sympathetic fibers. Noradrenergic tone is
blocked upon activation of the parasympathetic system and the intralacunar
smooth muscle relaxes. Blood flows easily into the relaxed lacunar space
through the helicine arteries. This distends the lacunar space and the
subtunical venules and emissary veins are physically compressed by the expanded
lacunae. In essence, the lacunar space becomes a large vascular “sink.” Blood readily flows into this sink, but it is unable to exit via the
penile venous system. Distension increases until the intralacunar pressure
equals the mean arterial pressure.
Regulation of cavernosal smooth
muscle is central to control of an erection. Simultaneous parasympathetic
neural pathway activation and inhibition of sympathetic outflow are required
for the smooth muscle relaxation that allows blood to flow into the sinusoidal
spaces (Fig. 13.1b). The parasympathetic nervous innervation travels to the
penis through the pelvic nerve whereas the sympathetic innervation travels in
the hypogastric nerve. Numerous neurotransmitters are involved in the
parasympathetic modulation of cavernosal smooth muscle relaxation. Nitric
oxide is the primary proerectile neurotransmitter. It colocalizes with
acetylcholine and vasoactive intestinal peptide (VIP) in nerve fibers
terminating on the trabeculae of the corpora cavernosa and on the helicine
arteries. Cavernosal smooth muscle contraction appears to be largely under α-noradrenergic
control. Norepinephrine is the major antierectile agent.
Reflex erection can be elicited
by afferent signals from sensory nerve endings on the glans; this reflex is
mediated at the level of the spinal cord. The afferent limb of the reflex is
carried by the internal pudendal nerves, which can also be activated by tactile
stimulation of the perineum near the testes and scrotum. Erections can be
modulated by supraspinal influences in the central nervous system. For
instance, serotonergic pathways within the raphe nucleus of the midbrain can
inhibit erections. The amygdala and the medial preoptic area of the
hypothalamus appear to be important higher integrating centers in the
modulation of erection. Dopamine is the candidate neurotransmitter in erectile
control at this level.
The importance of testosterone in
erectile function is not known. Nocturnal erections, which occur during
episodes of rapid eye movement (REM) sleep, are testosterone dependent. In
contrast, erections that occur in response to visual stimuli are not dependent
on testosterone and will occur in hypogonadal men.
As ejaculation approaches, penile
turgor increases even more. The smooth muscles in the prostate, vas deferens
and seminal vesicles contract sequentially to expel the seminal plasma and
spermatozoa into the urethra in a process known as emission.
Emission is mediated by α-adrenergic sympathetic fibers that travel through the
hypogastric nerve. Although emission and ejaculation are sometimes discussed as
a single entity under the term ejaculation, these processes are distinct;
ejaculation describes the ejection of semen from the posterior urethra. Ejaculation
requires contraction of the smooth muscles of the urethra and the striated
bulbocavernosus and ischiocavernosus muscles. These contractions are controlled
through a spinal reflex mediated by the pudendal nerve and spinal nerves 2, 3
and 4 (Table 13.1).
Hormonal control of spermatogenesis Although ongoing spermatogenesis in the testes can be maintained
qualitatively by testosterone alone, follicle-stimulating hormone (FSH) is
required for initiation of spermatogenesis. The primary site of action of FSH
within the seminiferous epithelium is in the Sertoli cells. FSH is delivered to
the interstitial area of the testis via small arterioles. Once there, it
diffuses through the basement membrane of the seminiferous tubules and binds to
specific plasma membrane receptors on Sertoli cells. Activation of the FSH
receptors results in the synthesis of both intracellular androgen receptors and
androgen- binding protein (ABP). ABP is secreted from the Sertoli cells and
binds androgens that have been produced by Leydig cells and diffused from their
interstitial site of production into the seminiferous tubule. ABP transfers
these androgens to the germ cells. Here, the androgens will be retained in the
promeiotic germ cells that contain androgen receptors. Once FSH initiates
spermatogenesis, the process will proceed as long as an adequate and
uninterrupted supply of testoster- one is available.
The FSH dependence of the Sertoli cells is analogous to the FSH
control of the homologous granulosa cells in the ovary. Like follicular phase
ovarian granulosa cells, Sertoli cells also secrete inhibin and activin. Inhibin, along with testosterone, inhibits
pituitary FSH secretion in the male. Activin receptors have been identified on
spermatogenic cells and may be involved in the FSH-mediated initiation of
spermatogenesis.
Leydig cell function
Like the homologous theca cells
in the ovary, Leydig cells respond to luteinizing hormone (LH) by synthesizing
and secreting testosterone in a dose-dependent manner. In addition to LH
receptors, receptors for prolactin and inhibin are found on Leydig cells. Both
prolactin and inhibin facilitate the stimulatory activity of LH on testosterone
production; neither can do this in isolation.
Regulation of gonadotropin secretion in males
The neuroendocrine mechanisms
that regulate testicular function are fundamentally similar to those that regulate
ovarian function. Hypothalamic gonadotropin-releasing hormone (GnRH), secreted
in a pulsatile fashion into the pituitary portal system, acts on the pituitary
of the male to stimulate synthesis and release of the gonadotropins, FSH and LH
(Chapter 1). These two gonadotropins regulate the spermatogenic and endocrine
activities of the testis. The male and female utilize the same negative
feedback mechanisms to inhibit gonadotropin release by the pituitary. However,
there is a major difference between regulation of the male and female
hypothalamic–pituitary–gonadal systems. The postpubertal male has continuous
gametogenesis and testosterone production while the postpubertal female has
cyclic functions. The lack of cyclicity in males occurs because androgens do
not exert a positive feedback on gonadotropin release.
Testosterone is the major
regulator of LH secretion in the male. The negative feedback effect of
testosterone is achieved largely by decreasing the frequency of the GnRH pulses
released by the hypothalamus; although there are minor reductions in GnRH pulse
amplitude. Testosterone also inhibits FSH release but its effects are not as
pronounced as they are on LH. Combinations of testosterone and the Sertoli cell hormone inhibin are required to produce
maximal FSH suppression.
