OJHAS Vol. 8, Issue 1: (2009
Biology of Sexual Dysfunction
Anil Kumar Mysore Nagaraj,
Lecturer, Dept of Psychiatry, K S Hegde Medical Academy, Mangalore, India,
Nagesh Brahmavar Pai,
Associate Professor, Graduate School of Medicine, University of Wollongong, Australia,
and Head, Dept of Psychiatry, K S Hegde Medical Academy, Mangalore, India,
Telat Srinivasarao Sathyanarayana Rao,
and Head, Dept of Psychaitry, J S S Medical College, Mysore, India,
Central Institute of Psychiatry, Ranchi, India
Anil Kumar Mysore Nagaraj,
Address For Correspondence
Lecturer, Dept of Psychiatry,
K S Hegde Medical Academy,
Anil Kumar MN, Pai NB, Rao S, Rao TSS, Goyal N. Biology of Sexual Dysfunction. Online J Health Allied Scs.
Submitted: Oct 13, 2008; Suggested
review Jan 12, 2009; Resubmitted: Jan 22, 2009 Accepted: Apr
9, 2009; Published: May 5, 2009
is a multifaceted activity, involving complex interactions between the
nervous system, the endocrine system, the vascular system and a variety
of structures that are instrumental in sexual excitement, intercourse
and satisfaction. Sexual function has three components i.e., desire,
arousal and orgasm. Many sexual dysfunctions can be categorized according
to the phase of sexual response that is affected. In actual clinical
practice however, sexual desire, arousal and orgasmic difficulties more
often than not coexist, suggesting an integration of phases. Sexual
dysfunction can result from a wide variety of psychological and physiological
causes including derangements in the levels of sex hormones and neurotrensmitters.
This review deals with the biology of different phases of sexual function
as well as implications of hormones and neurotransmitters in sexual
Key Words: Sexual dysfunction, Hormones, Neurotransmitters
is a multifaceted activity, involving complex interactions between the
nervous system the endocrine system, the vascular system and a variety
of structures that are instrumental in sexual excitement, intercourse
and satisfaction.(1) Sexual function is our physiological capacity
to experience desire, arousal and orgasm. Normal sexual function requires
the integrity of the genitalia, the reliable co-ordination of blood
flow, the activation of various smooth and skeletal muscles and the
stimulation of local secretions. This is linked with cognitive processes
attending to the sexual meaning of what is happening. Problem anywhere
in the entire sequence may lead to sexual dysfunction. Sexual dysfunction
can result from a wide variety of psychological and physical causes. Pathophysiology of sexual dysfunction involves derangements in the levels
of sex hormones and neurotransmitters.
by Kaplan, this consists of three phases- desire, arousal (excitement)
and orgasm.(2) However, the division is arbitrary and it only helps
to organize clinical and research oriented problems involving sexuality.
In clinical practice sexual desire, arousal and orgasmic difficulties
more often than not coexist, suggesting an integration of phases.
is a complex construct involving physiologic, cognitive, behavioural,
developmental and cultural components,(3) which are thought of as the
broad interest in sexual experiences including thoughts, fantasies,
dreams and wishes along with an interest in initiating or engaging in
sexual activity and frustration due to lack of opportunity for sexual
expression.(1) This stage is hypothetically a dopaminergic phenomenon
mediated by mesolimbic dopaminergic "reward centre" including
medial preoptic area (MPA) and anterior hypothalamus. The reward centre
receives inputs from serotonergic and noradrenergic neurons and contains
dopaminergic cell bodies.(4) Other contributing factors include testosterone
and oxytocin, as well as personality characteristics and psychosocial
arousal is characterized by a subjective sense of sexual excitement
associated with observable physiological changes such as penile tumescence
in men and pelvic vasocongestion, vaginal lubrication and swelling of
external genitalia in women. These responses may be accompanied in both
sexes by other bodily changes like skin flushing, tachycardia etc.(5)
penile erections are mediated by impulses descending from the cerebral
cortex and limbic system to reach thoracolumbar sympathetic ganglia
(inferior hypogastric plexus) and sacral parasympathetic ganglion.(6)
Baseline non-erect state is maintained by tonic adrenergic stimulation
adrenoceptors.(7) The sacral plexus via the pudendal and perineal nerves,
initiates tactile reflexogenic erections. Hypogastric plexus mediates
psychogenic penile erections. Efferent impulses from the parasympathetic
vasodilator fibers in sacral plexus initiate vasodilatory mechanism
for penile erection.(8)
sexual arousal in women begins with increased clitoral length and diameter,
and vasocongestion of the vagina, vulva, clitoris, uterus, and possibly
the urethra. Pelvic nerve stimulation results in clitoral smooth muscle
relaxation and arterial smooth muscle dilation. With sexual arousal,
there is an increase in clitoral cavernosal artery inflow and an increase
in clitoral intracavernous pressure that leads to tumescence and extrusion
of the clitoris. Engorgement of the genital vascular network increases
pressure inside the vaginal capillaries and results in lubrication of
the epithelial surface of the vaginal wall. The neurotransmitters that
mediate clitoral and arterial smooth muscle dilation remain undetermined.(9)
Orgasm in both sexes is characterized by climax of sexual pleasure associated
with rhythmic contractions of perineal muscles, cardiovascular and respiratory
changes and a release of sexual tension.(3)
men, there are two physiological stages of orgasm – (i) Emission,
involves the propulsion of seminal fluid to the bulbar urethra by the
contraction of the smooth muscles of the vas deferens, prostate and
seminal vesicles. This process is thought to be under the control of
thoracolumbar sympathetic nerves which release norepinephrine on to
alpha receptors. After emission, the external sphincter is opened to
allow release of fluid. In the second stage, a local, parasympathetic,
sacral spinal reflex activates the striated muscles surrounding the
bulbar urethra, producing ejaculation. The rhythmic contraction of these
muscles propels the semen outward. It is unclear to what degree the
occurrence and intensity of orgasm are shaped by central neurochemical
and cognitive processes.(5) Smooth muscle controlled emission and striated
muscle determined ejaculation involve separate nerve inputs and can
be pharmacologically distinguished.
women less is known about the neural mechanisms of orgasm and the process
is assumed to be largely similar to that in the male. Women are capable
of experiencing multiple orgasms in rapid succession, without the more
prolonged refractory periods. Mechanisms that make this possible are
not clear, although it is hypothesized that women are less sensitive
to the post-orgasmic secretion of prolactin that is hypothesized to
produce a refractory period in men and women.(10)
women ejaculate fluid from the urethra with orgasm. Chemical analysis
of this fluid confirms that while it may be mixed with small amounts
of urine, it is predominantly a secretion from the paraurethral glands,
thought to be a vestigial equivalent of the prostate. But this goes
unrecognized when it occurs in a retrograde direction.(11)
pituitary, adrenal and sex hormones in Sexual function
estrogen, progesterone, prolactin oxytocin, cortisol, pheromones are
the various hormones implicated in sexual function.
has been shown to restore nocturnal penile tumescence responses in hypogonadal
men, in whom this is impaired.(12) A recent study showed testosterone
increased sexual arousal and enjoyment among hypogonadal and normal
men, and had a positive effect on mood only among men with abnormally
low testosterone levels.(13) In normal adult males, there exists wide
individual variability in circulating testosterone levels that do not
seem to be linked in any meaningful, way with individual differences
in levels of drive or sexual behavior.(14) It is believed that the
level of testosterone required for sexual interest and activity in adult
males is lower than normal males’ circulating levels of testosterone.
Among males with normal testosterone levels, testosterone has not been
shown to facilitate erection.(15)
In an earlier
study of women who had undergone bilateral oophorectomy and adrenalectomy,
removal of the ovaries decreased sexual desire to a certain extent,
but removal of the adrenal glands had an even more deleterious effect
on desire.(16) Studies of surgically menopausal women generally indicate
that desire drops from presurgery level and may be restored with exogenous
administration of supraphysiological levels of testosterone with or
research suggests that estrogens have little direct influence on sexual
desire in either males or females. In men, relatively high levels of
exogenous estrogen have been somewhat effective in inhibiting sexual
desire among sex offenders and men who experience uncontrollable sexual
urges.(18,19) In women, some early studies have claimed that estrogen
(especially estradiol) is important for normal sexual desire, but most
current researches agree that estrogens play only a minimal role in
female sexual desire.(20,21)
deficiency, as occurs with menopause, causes a decrease in genital vasocongestion,
lubrication and atrophy of the vaginal epithelium. Such changes not
only impair the physiological sexual arousal response in women and may
cause dyspareunia (painful intercourse), but can adversely influence
the psychological experience of sexual arousal. These changes could
be expected to indirectly impair sexual desire.(22)
studies have revealed a decrease in sexual desire in men receiving intramuscular
injections of progesterone.(23,24) No controlled studies have been
conducted on the relationship between progesterone treatment and sexual
desire in men.
oral contraceptives that increase
progesterone levels throughout the menstrual cycle in female have been
associated with decreased sexual interest and desire.(25,26)
It is generally agreed on, however, that progesterone treatment does
not have a substantial influence on the sexual desire of either premenopausal
or postmenopausal women.(17,27,28)
and women with abnormally high levels of prolactin report a decrease
in sexual interest that is restored with bromocriptine treatment.(29)
It is unclear whether the reversal of sexual symptoms secondary to bromocriptine
treatment is attributable to the lowering of serum prolactin levels,
to the correction of hypothalamic dopaminergic dysregulation, or to
an interaction between these two mechanisms.(30)
Prolactin's effect on other aspects
of human sexual behaviour remains equivocal. Erectile dysfunction has
been described in men with abnormally high levels of prolactin, (31)
but has also been described in men with unusually low levels of prolactin,
(32) suggesting more than a simple inhibitory role of prolactin on erectile
ability. In women, abnormally high levels of prolactin have been associated
with amenorrhoea, infertility and decreased sexual ability.(33)
levels of oxytocin increase during sexual arousal and orgasm in both
men and women.(34) Using a continuous blood sampling technique and
electromyography, it was reported to have a positive correlation between oxytocin levels and the intensity, but not the duration of orgasmic
contraction in males and females.(35) Most of what we know about the
influence of oxytocin on sexual behaviour however is based on animal
(Cushing syndrome) can produce a constellation of symptoms including
depression, insomnia and decreased libido in males and females. Cortisol
levels were higher in men with psychogenic erectile dysfunction who
demonstrated a poor response to intracavernosal injection of a smooth
are substances secreted from glands at the anus, urinary outlet, breasts
and mouth. In a recent double blind, placebo-controlled study, it was
reported that women exposed to a synthesized human male pheromone reported
higher levels of sexual intercourse, sleeping with a romantic partner,
but no change in masturbation frequency. The authors interpreted these
findings as evidence for male pheromones increasing the sexual attractiveness
of men to women.(37)
neurotransmitters in sexual function
oxide, serotonin, dopamine, epinephrine, norepinephrine, acetylcholine,
histamine, GABA are all implicated to have roles in sexual function.
Neurotransmitters act both within the brain and in peripheral organs,
and therefore may play complex and interacting roles in promoting and
facilitating sexual functioning.
oxide (endothelial relaxing factor)
oxide (NO) is an essential component in the production of penile, and
possibly, clitoral vasocongestion and tumescence. The release of NO
by cholinergic and non-cholinergic nerves appears to be the major contribution
of the parasympathetic nervous system.(38) As described above, NO is
now understood to be the most significant mediator of vascular smooth
muscle relaxation, responsible for engorgement of erectile tissue in
men and women.
stimulation leads to NO production that in turn stimulates the release
of guanylate cyclase. Guanylate cyclase converts guanosine triphosphate
to cGMP and cGMP produces relaxation of the smooth muscles of the penile
arteries and corpus cavernosum resulting in increased blood flow into
the penis.(39) Some evidence suggests that this may also occur in the
cGMP is metabolized by cyclic nucleotide phosphodiestrase isozymes into
gunanosine 5'- monophosphate. As long as sexual stimulation continues,
cGMP production and metabolism remain balanced and penile or clitoral
tumescence is sustained.(41) Erectile dysfunction can result when this
process is not working normally or when it is partially or completely
Intestinal Polypeptide (VIP)
has been less well understood but is shown to co-localize with NO is
nerves to genital blood vessels and smooth muscle. In women, systemic
administration and local subepithelial injection of VIP result in increased
vaginal blood flow and lubrication.(9) In addition, sexual arousal
raises the level of VIP found in the plasma. In men VIP also co-localizes
with NO and has been shown to play an important role in erection.(5)
acts at both central and peripheral receptors in the mediation of sexual
serotonin appears to downregulate and diminish levels of mesolimbic
dopaminergic activity and to elevate prolactin, resulting in decreased
libido.(42,43) In addition, serotonergic activation of different receptor
subtypes has differential effects on sexual functioning. Activation
of receptor subtype IA lowers the thershold for ejaculations,
while activation of 2A, 1B or IC
inhibits sexual behaviours and stimulation of 2C facilitates
behaviour in animal models.(44)
at spinal or end-organ receptors, serotonin has inhibitory effects on
ejaculation in animals.(45) Also serotonin tends to cause problems
with orgasm and desire more than arousal itself. Serotonin even acts
on the smooth muscles of the genitals possibly inhibiting the muscular
contractions that characterize orgasm.(5) Further, serotonin acts at
peripheral nerves, where it appears to affect the flow of genital sensory
information. Lastly, serotonin may delay orgasm through pre-synaptic
inhibition of adrenergic transmission.(45)
the four major dopaminergic CNS pathways are proposed to play a role
in sexual behavior. The incertohypothalamic pathway stimulation increases
all phases of male rat sexual behaviour and induces penile erection.
In female rats it induces sexually receptive posture called lardosis.
The mesolimbic pathway is involved in the anticipatory phase of sexual
activity associated with motivation and sexual reward. The nigrostriatal
pathway is important in the motor behaviour required for consummatory
sexual activity in male rats. Lastly the tubero infudibular pathway
appears to play a role in baseline sexual interest as opposed to more
acute behavioural changes.(5,46,47)
relationship between dopamine and prolactin, it remains unclear whether
hyperprolactinemia itself is causative or acts as a surrogate marker
for decreased dopmine. A recent F-MRI study demonstrated an increase
in blood flow to specific dopaminergic and other brain structures when
17 college men and women viewed pictures of people they love and are
sexually attracted to.(48)
levels of epinephrine have been shown to increase prior to viewing an
erotic film, slowly increase during masturbation, peak at orgasm, and
return to baseline level within several minutes of orgasm.(49) The
epinephrine and norepinephrine metabolite, vanillylmandelic acid, increases
prior to intercourse and continue to be elevated over baseline upto
23 hours following sexual activity.(50)
men, blood plasma NE levels were positively correlated with arousal
and erection during masturbation and sexual activity, increased upto
12-fold at orgasm and declined to baseline levels within 2 minutes of
reaching orgasm.(51,52) Studies suggest that NE is also active during
the sexual response cycle of women. Blood plasma levels of NE increased
during masturbation, peaked at orgasm, and slowly declined following
orgasm in normally functioning women.(49,52)
occurs when the smooth muscles of the corpus cavernosum relax permitting
increased blood flow into the penile tissue. The human corpus cavernosum
is innervated by cholinergic nerves and contains cholinergic receptors
suggesting endogenous cholinergic activity in the penile tissue.(53,54)
(Ach) appears to play a less direct role in sexual functioning that
is largely a function of maintaining the balance of cholinergic and
sympathetic input at the genital level.(5) Ach antagonist, atropine
showed no effect on either vaginal vasocongestion or orgasm in women
and large doses were insufficient to block penile erection in men,(9)
though in vitro administration of Ach to pre-contracted corpus cavernosum
induced smooth muscle relaxation.(7) Thus Ach is sufficient to produce vasocongestion, but not essential for this effect.
are three proposed roles for cholinergic stimulation in promoting sexual
- Alteration of the
balance of sympathetic and parasympathetic inputs.(7)
- Facilitation of
lubrication by increasing secretions.(55)
- Synthesis and secretion
of NO and VIP, that are essential for arousal.(5)
little is known about the role of histamine in facilitating sexual functioning,
but evidence suggests that activity at both H2
and H3 receptors in the penis can cause erection.(56) There
are a few case reports of decreased desire in both men and women taking cimetidine (H2 antagonist), the mechanism of which may be,
decreased peripheral response to testosterone (7) or decreased metabolism
of estradiol leading to gynaecomastia in men.(57)
aminobutyric acid (GABA)
enhancing benzodiazepine use has been implicated in case reports of
decreased libido, erectile dysfunction and anorgasmia.(58) While mechanisms
are poorly understood, it is hypothesised that centrally mediated sedation
and peripheral muscle relaxation may be responsible.(5)
from the above mentioned ones, many other putative neurotransmitters,
including arginine-vasopressin, angiotensin II, substance P, neuropeptide-Y, a-MSH,
Gn RH are involved in sexual functioning, but there is little research
into their precise role.(59)
Table 1: Stages of
|The spontaneous occurrence of sexual
thoughts, fantasies, dreams and wishes, along with an interest in initiating
or engaging in sexual activity|
Peripheral or physical;
Central or subjective
|Genital (vascular engorgement and
lubrication) and systemic responses (tachycardia, hyperventilation;
etc.) to sexual stimulation.|
||Intense peak of sexual pleasure accompanied
by rhythmic contractions of the genital and reproductive organs|
||Return to baseline, unaroused state,
characterised by loss of vasocongestion in the penis and vulva|
Table 2: Summary of
Role of Hormones: (60)
Stage of sexual response
||Testosterone, Estrogen, Oxytocin
is a complex phenomenon involving an orchestra of chemical elements
ranging from small molecules like nitric oxide to peptides like oxytocin.
We are aware that derangements of various hormones and neurotransmitters
are involved in sexual dysfunction but their precise role is not known.
Further, putative neurotransmitters are gaining more implications in
sexual dysfunction. Deeper investigation into these areas will no doubt
reveal greater insight about sexual functioning which in turn assists
in efficient management of sexual dysfunction
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