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Impotence or, more clinical, erectile dysfunction is the inability to
maintain an erection of the penis for satisfactory sexual intercourse
regardless of the capability of ejaculation.
According to a recent survey, the Massachusetts Male Aging Study, 52%
of men beyond 40 years of age may have some degree of erectile failure.
Unfortunately, only a small percentage of men seek medical help.
Penile erection is managed by two different mechanisms. The first one
is the reflex erection, which is achieved by directly touching the
penile shaft and the second is the psychogenic erection, which is
achieved by erotic stimuli. The first one uses the peripheral nerves and
the lower parts of the spinal cord, whereas the second one uses the
limbic system of the brain. Neural signals originating in the limbic
system of the brain are transmitted through spinal cord to the
thoracolumbar erection center in the spine. Psychogenic erection is
associated with either fantasy or viewing erotic material. Reflex
erection occurs when signals triggered by touching the penile shaft are
carried through the pudendal nerve to S4-5 in the lower spinal cord.
Stimulation of S4-5 sends parasympathetic signals to the penis and leads to reflex erection. Both mechanisms augment
each other during sex. In both conditions an intact neurologic system is
required for a successful and complete erection. Stimulation of penile
shaft by the nervous system gives rise to the secretion of nitric oxide
(NO), which causes the relaxation of smooth muscles of corpora cavernosa
(the main erectile tissue of penis), subsequently giving rise to penile
Although neural signals are crucial, the vigor of a man?s erection is
ultimately determined by vascular events governing the flow of blood
into the corpora cavernosa. The force with which blood flows into the
corpora cavernosa is mediated by an intriguing intracavernosal chemistry
sequence involving the enzyme nitric oxide synthase (NOS), nitric oxide
(NO), and a second enzyme (adenylate cyclase), which helps generate the
cyclic guanosine monophosphate needed to maximize intracavernosal blood
flow and increase the pressure within the corpora cavernosa.
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The main neurotransmitter produced seems to be NO, the
endothelium-derived relaxing factor. This agent causes relaxation of the
arterioles and cavernosal smooth muscle of the penis, which allows
increased blood flow and increases the intracorporeal pressure to
approximate the systolic pressure. The dilated corpora compress the
venous outflow channels against the elastic tissue of the tunica
albuginea, an action that prevents venous leakage and further increases
the intracavernosal pressure to above systolic blood pressure. Just
before ejaculation, the ischiocavernosal and pubocavernosal muscles
contract to increase intracavernosal pressure further; the response is
Additionally, adequate levels of testosterone (produced by the
testes) and an intact pituitary gland are required for the development
of a healthy male erectile system. As can be understood from the
mechanisms of a normal erection, impotence may develop due to hormonal
deficiency, disorders of the neurologic system, lack of adequate penile
blood supply or psychological problems.
The role of testosterone in male sexual function remains complex and
controversial. Men acquire full sexual and reproductive competence at
adolescence when, in response to pulsatile pituitary luteinizing hormone
(LH) secretion, Leydig cell testosterone production surges to adult
levels as coincidental pulsatile pituitary folliclestimulating hormone (FSH)
secretion initiates and maintains
the orderly process of spermatogenesis in testicular Sertoli cells.
Thereafter, the role of testosterone becomes unclear. Some men
with below-normal testosterone levels can still have nocturnal
erections, but for fully satisfactory sexual and erectile function, a
?normal? quotient of
testosterone must be present in the bloodstream.
As testosterone levels decline, so does a man?s sexual function. Two
actions of testosterone?one central and the other peripheral?are thought
to be critical. Testosterone is the main hormonal mediator of a man?s
libido. As testosterone levels decline, sexual desire decreases.
Testosterone also has a critical role in stabilizing the levels of
intracavernosal NOS, the enzyme responsible for triggering the NO
cascade required to have an erection. Thus, the man with inadequate
circulating testosterone will have a dampened libido and suboptimal
erectile function. Anything that interferes with hypothalamic pulsatile
LH release or reduces the number of Leydig cells available to respond to
LH will result in decreased production of testosterone.
Usually, both mechanisms are at work to cause erections, but as men
age, they derive less stimulation from the higher centers and need to
rely more on direct penile stimulation hence, the requirement of aging
men to practice extended foreplay. The mechanisms involved are complex
and may be related to decreased production of or responsiveness to NOS,
the enzyme that produces NO.
Erections, once achieved through fantasy and foreplay, are more
fragile as men age. Older men must maintain their focus; if they become
distracted by thinking of work or other activities, detumescence may
occur. The telephone ringing may be enough to cause detumescence.
As men age, the absolute number of Leydig cells decreases by about
40%, and the vigor of pulsatile LH release is dampened. In association
with these events, the free testosterone level declines approximately
1.2% per year and may be associated with commensurate increases
in serum LH levels. Most aging men with subnormal levels of
testosterone, however, have low or inappropriately normal levels of LH.
Some clinicians believe that ageappropriate but lowered levels of free
testosterone (in comparison with those in young men) are not
contributory to sexual dysfunction. Nevertheless, some clinical studies
have substantiated positive responses to testosterone therapy in men
with borderline low levels of free testosterone.
- Diseases of the blood vessels (vascular disease) e.g.
arteriosclerosis, hypertension, high cholesterol.
- Diabetes can damage both blood vessels and nerves.
- Neurologic disorders affect the nervous system and include
multiple sclerosis, Parkinson's disease and spinal cord injury with
- Deficiencies of the endocrine system for example, low levels of
testosterone or thyroid hormone often cause poor quality erections.
Excessive production of prolactin by the pituitary gland may
contribute to a low testosterone level and lack of desire.
- Substance abuse affects erectile function as well. Illegal drugs
and the excessive use of alcohol or cigarettes can seriously damage
the blood vessels and nerves involved in a normal erection.
A few causes of impotence may be iatrogenic (medically caused).
Various medications intended to control blood pressure or to modify
central nervous system response, may inhibit erection by denying blood
supply or by altering nerve activity. Surgical intervention for a number
of different conditions may remove anatomical structures necessary to
erection, damage nerves, or impair blood supply. Radical pelvic surgery
may also result in impotence. Surgical procedures involving the prostate
gland the bladder or colon may sever the nerves involved in erectile
response. Radiation treatment in this area can also affect the erectile
Erectile dysfunction is characterised by the inability to maintain
erection. Normal erections during sleep and in the early morning suggest
a psychogenic cause, while loss of these erections may signify
underlying disease, often cardiovascular in origin. Other causes leading
to erectile dysfunction are diabetes mellitus (causing neuropathy) or
hypogonadism (decreased testosterone levels due to disease affecting the
testicles or the pituitary gland).
There are no formal tests to diagnose erectile dysfunction. Some
blood tests are generally done to exclude underlying disease.`
Treatment depends on the cause. Testosterone supplements may be used
for cases with hormonal deficiency. However, usually the cause is lack
of adequate penile blood supply as a result of age-dependent damage of
inner walls of blood vessels. Previously, medical substances (e.g.
apomorphine) were used to be directly injected into the erectile tissue
of penile shaft to treat impotence. In some cases refractory to the
medical treatment, a penile implant (penile prosthesis) could be
advised. After the discovery of orally active agents that increase the
efficacy of NO, which dilates the blood vessels of corpora cavernosa,
more conservative methods were started to be used.
Sildenafil citrate (Viagra?) is an oral agent that blocks specific
phosphodiesterases. NO acts on blood vessels by increasing the levels of
cyclic guanosine monophosphate, which is required for dilation of the
vessels. Phosphodiesterases block this substance and reduce the effect
of NO on erectile tissue. By using sildenafil, NO's effects are
increased and a more sustained penile erection can be achieved. Other
agents with less side effects and holding promise as an effective oral
treatment for penile erectile dysfunction are currently being developed.
Two newer drugs now available for the treatment of erectile dysfunction
are tadalafil (Cialis?) and vardenafil (Levitra?). These agents have a
similar mode of action to Sildenafil.
A double-blind study appears to show evidence that ginseng is better
than placebo: see the ginseng article for links and more details.