Introduction
The physiology of human
sexual function
Roy Levin
Alan Riley
Abstract
The terminology for the complexities of human sexual activity is dis-
cussed and the male and female sexual arousal to orgasm is described
with its underlying physiological mechanisms. The original four-phased
human sexual response cycle of Masters & Johnson (Excitation, Plateau,
Orgasm, Resolution) is now modified by amalgamation of the plateau
phase into the excitation phase and the addition of two desire ­phases,
one spontaneous (proactive) the other activated by arousal per se (re-
active). The relation between genital arousal and subjective arousal
is reviewed for males and females. In males, erection and subjective
arousal usually have good concordance but in females increased vaginal
blood flow and lubrication can occur without any concomitant subjective
arousal even with sexually aversive stimuli. The subjective feeling of
sexual arousal in women is now regarded as more complex than stimuli
from the genitals, involving the contextual meaning and content of the
stimuli. Imaging studies have revealed multiple areas of the brain that
become involved during sexual arousal and at orgasm. However, differ-
ent studies using different techniques and analyses have given conflict-
ing accounts of which areas are activated and which are deactivated, and
it is not possible at present to finalize the position.
Keywords brain imaging; clitoris; ejaculation; emission; erection; ­female
ejaculation; orgasm; sexual arousal; sexual desire; sexual ­response ­cycle;
vaginal lubrication
Human sexual activity involves a complicated interaction of
physiological, psychosocial and behavioural components in
and between individuals.1 Over the last 20 years, significant
advances have been made in our understanding of the physiol-
ogy of human sexual functioning, especially at the peripheral
level. We are now also beginning to investigate and study the
Roy Levin MSc Phd is Honorary Research Associate at the Sexual
Physiology Laboratory, Porterbrook Clinic, Sheffield, UK. Previously he
was Reader in Physiology in the Department of Biomedical Science,
University of Sheffield from 1977 until his retirement in 2000. Conflicts
of interest: none declared.
Alan Riley MRCS DObstRCOG FFPM was Professor of Sexual Medicine at the
Lancashire Postgraduate School of Medicine and Health, University
of Central Lancashire, Preston, UK until his retirement in 2006. He
qualified from the University of London in 1967 and has specialized
in sexual medicine for the past 36 years. Conflicts of interest: none
declared.
PSYCHIATRY 6:3
What’s new?
• The original four-phased human sexual response
cycle (EPOR) of Masters and Johnson is now modified
by amalgamation of the plateau (P) phase into the
excitation (E) phase and the addition of two desire
phases, one spontaneous (proactive) the other activated
by arousal (reactive)
• Increased vaginal blood flow and lubrication can occur
without concomitant subjective arousal even with
aversive stimuli
• Descriptions of brain imaging of the areas activated
or deactivated during sexual stimuli using different
techniques and analyses have given conflicting
conclusions and a consensus is as yet unavailable
central mechanisms involved. Knowledge of the sexual physiol-
ogy is essential if we are to understand the biological causes and
management of sexual dysfunction.
The terminology of human sexual activity
Many authors use the terms ‘sexual arousal’ and ‘sexual excite-
ment’ synonymously but it is useful to keep sexual arousal (a
state) to denote physiological changes and sexual excitement as
the subjective awareness of the arousal. Greater difficulty occurs
when it comes to describing the central mental process creating
the subjective awareness of arousal. The literature has sexual
drive, desire, interest, appetite, motivation and libido (see Levin2
for a detailed discussion). Sexual drive is the ‘biological’ drive
while sexual desire can be thought of as an object-focused drive –
we desire to participate in a particular type of activity or with
a particular partner. This dichotomization has been helpful in
understanding sexual desire problems.3 Sexual desire can occur
without sexual arousal and sexual arousal without sexual desire.
An important reinforcer for sexual desire is sexual satisfaction.
People differ in their criteria for sexual satisfaction, but a work-
able definition is how close the actual sexual experience was
compared to its expectation.
In men erection usually serves as an index of subjective
arousal (sexual drive/desire) although immediately after ejacula­
tion most have genital arousal but no sexual desire: desire is
discharged before arousal. In women, however, genital arousal
is not always commensurate with subjective arousal or with the
degree of subjective arousal. Women can show genital arousal
(increased blood flow and lubrication) to various sexual stimuli,
even those that they dislike, without having any corresponding
subjective arousal. The increased blood flow of genital arousal
appears to be an automatic response to various sexual stimuli.
The subjective feeling of sexual arousal in females is now real-
ized to be a more complicated cognitive process involving the
stimulus meaning and content than simply from the signal of an
aroused genitalia, especially during longer-term relationships.4
90 © 2007 Elsevier Ltd. All rights reserved.
 Introduction
Sexual response cycle
The sequence of events that characterizes the progression from
the sexually unaroused to the aroused state and the resolution of
these changes is described as the human sexual response cycle,5
with genital and non-genital components. The latter include
increased heart rate, blood pressure and respiration, nipple erec-
tion, myotonia and dilated pupils.
The biological purpose of the sexual response in men is to
enable sperm to be introduced into the vagina, while the genital
changes occurring in women facilitate painless penile penetra-
tion and thrusting, at the same time providing erotic sensations
and ensuring optimal reproductive fitness (sperm survival and
transport). The latter function is not considered in this contribu-
tion but the role of sexual arousal in human sexual reproduction
is the subject of a recent review.6
Based on observations of the sexual responses of men and
women in their laboratory, Masters and Johnson identified
four phases, namely: Excitement (E), Plateau (P), Orgasm (0)
and Resolution (R) – the EPOR model5 – but they neglected to
include a phase that initiated sexual activity. Most people do not
suddenly become sexually active; they normally experience an
initiating phase of sexual desire (D). This can come about either
spontaneously (proceptive desire – D1) or by activation through
sexual excitation (responsive desire – D2); the mechanisms of D1
and D2 are not necessarily different but are initiated at different
times. The original EPOR model has now become modified as
the DEOR model (or more accurately the D1D2EOR model) as it
has become clear that the Plateau or P-phase was misnamed and
unnecessary because it was actually a phase of increasing sexual
excitement, basically, the end of the E-phase into which it has
now been incorporated (see Levin for a review on the develop-
ment of the human sexual response model7).
Sexual stimulation
The sexual response activated by effective sexual stimulation can
be viewed as the algebraic sum of positive (sexually stimulating)
and negative (sexually inhibiting) stimuli. Sexually stimulating
factors may be psychogenic or reflexogenic. Psychogenic sexual
stimulation arises in the brain and may be triggered by input
from the special senses (vision, hearing, taste and smell) or by
consciously contrived sexual fantasies. Inhibiting factors can be
varied, such as religious feelings, guilt, shame, disgust, igno-
rance of sexual technique etc. Reflexogenic sexual stimulation
arises from genital stimulation and/or erotogenic sites (breasts,
nipples, inner thighs, perineum).
Spinal cord mechanisms
Sensory input arising from stimulation of the external genitalia is
conveyed in the pudendal nerve to the medial central grey matter
of the lumbosacral spine and the information is relayed to supra-
spinal sites in the spinothalamic and spinoreticular pathways.
Two different pathways carry the sensory information from the
glans via the dorsal nerve of the penis. The sensory fibres of
the pudendal nerve conveys the information to the spinal cord,
and the information also travels to the hypogastric plexus and
thence to the ganglia of the paravertebral lumbo-sacral sympa-
thetic chain. The concept of two interconnected central pattern
PSYCHIATRY 6:3
generators has been proposed from male rodent studies – one
for erection/emission (probably located at L2/L4) and one for
ejaculation (probably located at S1/S2). They are influenced by
descending signals from the brain that inhibit or activate them to
fire off.8 Whether a central pattern generator exists in the spinal
cord of females to activate the pelvic striated muscles at orgasm
is unknown.
Brain imaging during sexual arousal and orgasm
Apart from the very limited information available from subjects
with brain lesions, those with epilepsy and the rare cases of elec-
trical stimulation of the brain (see Levin2 for references), ani-
mal studies, especially in rodents, have been the major source
of information about the central mechanisms controlling sexual
arousal/behaviour. While numerous neurotransmitters are impli-
cated in the complex mechanisms of sexual activity (choliner-
gic, adrenergic, vipergic, oxyntergic, prolactinergic), studies in
rats have yielded a simplified concept that dopaminergic trans-
mission is pro-sexual and facilitates sexual motivation, sexual
arousal and reward while serotonergic transmission is inhibitory
especially for ejaculation. However, the role of dopamine as a
specific promoter of sexual behaviour has been strongly chal-
lenged: the argument forwarded is that it simply acts by being
the activator of motor functions and general arousal.9 Species
differences always pose a possible problem. It is now known that
areas in rodent brains activated during ejaculation (medial pre-
optic area and amygdala) are not activated in humans.10
The advent of brain imaging by measuring changes in regional
cerebral blood flow (rCBF) or metabolism by functional mag-
netic resonance imaging (fMRI) or by blood oxygenation level
dependent-positron emission tomography (BOLD-PET) as indi-
ces of neuronal activation has revolutionised our ability to map
activity in areas of the human brain. One difficulty, however,
is that while we now know what areas are activated or deac-
tivated during sexual arousal/orgasm we have relatively poor
understanding of exactly what tasks each area performs in rela-
tion to the arousal, and what exactly is the response specific
to sexual arousal.11 Many areas are multifunctional (e.g. the
amygdala), activated by diverse stimuli viz pain, pleasure, anger,
fear, emotional processing etc. Also, it is not known whether
activation of an area involves all or a highly selected number of
neurons as spatial resolution is poor. Nevertheless, brain imag-
ing has significantly advanced our conception of central brain
sexual mechanisms. The presumption of a single site for arousal/
orgasm had to be abandoned when multiple site co-activation
during arousal/orgasm became obvious. Comparisons are diffi-
cult because of a lack of standardized criteria for what consti-
tutes significant activation over the basal levels and because of
different methodologies of arousal and recording. While many
features of brain activation during sexual arousal are common
to men and women, the amygdala and hypothalamus are more
strongly activated in men when viewing identical sexual stimuli
even though the women reported greater sexual arousal.12 Direct
sexual stimulation of the penis, in a study by Georgiadis and
Holstege,13 activated a number of areas including the posterior
second somatosensory cortex and the insula, but no activity was
seen in the thalamus or hypothalamus and a reduction occurred
in the amygdala. Of the few imaging studies of arousal in normal
91 © 2007 Elsevier Ltd. All rights reserved.
 Introduction
men and women, only two feature orgasm and that in women
has only been briefly reported.
According to Holstege et al.,10 the most strongly primary acti-
vated region of the brain during male erection/orgasm is the
region of the ventral tegmental field, the midbrain lateral central
tegmental field, the zona incerta, the suprafascicular nucleus,
the ventroposterior, midline and intralaminar nucleus and the
cerebellum. Other parts showing activation were the lateral puta-
men, adjoning parts of the claustrum and neocortical activity on
the right side. No activation was seen in the hypothalamus and
preoptic area, while decreased activation was seen the amygdala
and adjacent entorhinal cortex. Interestingly, the amygdala also
shows decreased activity when volunteers viewed pictures of
their deeply loved ones and in those experiencing cocaine ‘rush’.
Holstege suggested that euphoric states create the deactivation
but he also claimed that it occurred even during sexual stimula-
tion and erection (hardly euphoric states).8
Only a brief conference account of brain activation during
orgasm in women has been reported by Holstege (see Levin14).
The pattern was said to be similar to male study10 except that the
amygdala and the periaqueductal grey were claimed to be acti-
vated. Komisaruk and Whipple reviewed their imaging studies on
the induction of orgasm (thought to be via the vagus) in 4 paraple-
gic women, and also their preliminary findings in women who
could create orgasm by mental activity alone. In the paraplegic
women a large number of sites, including now the hypothalamus,
were activated by the cervical stimulus used to create arousal to
orgasm, but in the women who used only thoughts to activate their
orgasms only the regions of the paraventricular nucleus, hippocam-
pus and anterior cingulate cortex were activated. This suggested to
them that these sites may be specifically related to orgasm. In these
subjects the amygdala was not activated by orgasm.15
It is clear that it is not possible at present to give a consensus
account of brain activation to sexual arousal in men and women
as the various studies have produced differing results and conclu-
sions, creating uncertainty in the field.11,12,14,16 For example the
amygdala, claimed to be deactivated at ejaculation, is described
as being activated during arousal.12 Holstege speculated that to
ejaculate the male has to have a general lack of fear – that’s why
it is deactivated!8
Genital arousal
Genital arousal in both sexes is essentially a vasocongestive and
neuromuscular event controlled by facilitatory parasympathetic
and inhibiting sympathetic neural mechanisms. The primary
changes are penile erection in men and clitoral tumescence, geni-
tal vasocongestion and increased vaginal lubrication in women.
The increase in heart rate and blood pressure that occurs during
sexual arousal provides the increased blood flow to the genitals.
Penile erection
Erection is a haemodynamic response in the two corpora cavernosa
and the corpus spongiosum. The corpora cavernosa are encased
in the firm sheath of the tunica albuginea, the structural integrity
of which is essential for normal erection. The corpora cavernosa
consist of erectile tissue in which there are multiple, interconnect-
ing lacunar (or cavernosal) spaces, walled by smooth (cavernous)
muscle and a fibro-elastic framework. The lacunar spaces are lined
PSYCHIATRY 6:3
by vascular endothelium and are supplied by the helicine arteries,
branches of the cavernous arteries. The lacunar spaces are drained
by venules located at the periphery of the erectile tissue. These
merge to form the emissary veins, which pass obliquely through
the tunica albuginea to drain into the circumflex veins.
The penis is maintained flaccid by contraction of the cav-
ernous muscle and constriction of the helicine arteries. This is
predominantly a sympathetically mediated event, with noradren-
aline activating α1-adrenoceptors on these structures. In response
to effective sexual stimulation relaxation of the cavernous mus-
cle occurs resulting in increased volume of the lacunar spaces.
At the same time, dilatation of the helicine and cavernosal arter-
ies occurs, allowing more blood to be delivered to the lacunar
spaces at systemic pressure. Initially, blood drains from the lacu-
nar spaces through the emissary veins but as the spaces fill up
and enlarge, the erectile tissue expands and the penis becomes
tumescent (swollen) but can still be bent. However, as the erec-
tile tissue expands further it comes up against the resistance of
the tunica albuginea, compression of the emissary veins occurs,
preventing further drainage. As a consequence, intracorporeal
pressure rapidly increases leading to full penile rigidity. The
organ now cannot be bent and can penetrate into the vagina.
Relaxation of the cavernous muscle and arterial dilatation is
brought about by decrease of cytoplasmic free calcium in the
smooth muscle cells. This is mediated by several mechanisms,
including withdrawal of sympathetic tone and the release of
vasoactive neurotransmitters. Nitric oxide (NO) appears to be
the most important; it is produced in response to sexual stimula-
tion by the enzyme nitric oxide synthetase in parasympathetic
nerve endings, and endothelial cells within the corpora. NO
activates guanosine triphosphatase, producing cyclic guano-
sine monophosphate (cGMP), which lowers intracellular free
calcium. cGMP is inactivated by phosphodiesterase 5 (PDE-5).
PDE-5 inhibitors facilitate erection by increasing the level of
cyclic GMP. Many other vasoactive neurotransmitters are in­­
volved in the erectile process, including prostaglandin E1 and
vasoactive intestinal polypeptide (VIP).
The increase in sympathetic activity that occurs during ejacu-
lation is probably instrumental in initiating detumescence, but
other vasoconstrictor neuropeptides are possibly also involved.
Clitoral tumescence
The mechanism and control of clitoral tumescence is similar to
that of the penis involving VIP and NO. The body of the clitoris
containing erectile tissue extends around the vagina and urethra
deep to the labia minora, giving rise to the vestibular bulbs, and
may extend into Halban’s fascia between the anterior vaginal
wall and the bladder.
Vaginal circulatory changes and lubrication
The vagina is a potential space lined by a squamous epithelium
devoid of glands. The epithelial cells have a limited capacity to
transfer sodium ions from the lumen to blood; this transfer powers
the osmotic reabsorption of vaginal fluid. The wall has two layers
of smooth muscle, an inner longitudinal layer (contraction short-
ens and widens the vagina) and an outer circular layer (contrac-
tion constricts the vagina). These muscles are under autonomic
nervous control and their tone is not consciously perceived. At
its distal end, the vagina is surrounded by the bulbocavernosus
92 © 2007 Elsevier Ltd. All rights reserved.
 Introduction
and ischiocavernosus (striated) muscles. The bulbocavernosus
muscle is more superficial and surrounds the vaginal introitus:
its contraction narrows the introitus. The ischiocavernosus mus-
cle extends from the ischial ramus and tuberosity of the pelvis to
either side of the introitus.
In the unaroused state the vaginal blood flow is minimal.
This is achieved by a high adrenergic tone and ‘vasomotion’, a
process where random opening and closing of capillaries occurs
to just satisfy local metabolic demands.6 The initial change that
characterizes vaginal sexual arousal is an increased blood flow
mediated by a reduction in the adrenergic tone and activation of
the VIPergic innervation with a small component of NO.17 More
capillaries become recruited and opened; when all are open with
increased flow the tissue is full of blood creating vasocongestion.
An increase in vaginal lubrication usually occurs within seconds
of the onset of sexual arousal created by neurogenic transuda-
tion, probably mediated by VIP and calcitonin gene-regulating
peptide, which increases the permeability of the capillaries.17
The ultrafiltered plasma transudate powered by the vasoconges-
tion permeates through the intercellular channels of the epithe-
lium saturating its limited sodium ion reabsorptive capacity and
leaking through, appearing as bead-like droplets on the surface
of the vaginal epithelium. These coalesce forming a thin lubricat-
ing surface film. The transudate, a slippery smooth fluid, prob-
ably picks up cervically secreted sialoproteins coating the vaginal
epithelium to give it its lubricating properties.
When arousal is high the distal end of the vagina balloons
out and the uterus is elevated away from the posterior vaginal
wall (vaginal tenting). This has been proposed as an important
feature of reproduction (see Levin6 for references).
Ejaculation and orgasm
Ejaculation in the male is the process by which spermatozoa con-
tained within seminal fluid are ejected forcefully from the ure-
thral meatus. Some women experience a discharge of fluid from
the urethra at orgasm and high levels of sexual arousal, often
by stimulation of the so-called G-spot on the anterior wall of the
vagina, and this has been termed ‘female ejaculation’. Whether
this discharge is urine or a product of the paraurethral glands or
a mixture of both continues to be debated.18
Emission and ejaculation
Four distinct events are involved:
• emission, during which the secretions of the testes, prostate,
seminal vesicles and the ampullary parts of the vasa deferen-
tia (containing spermatozoa) are deposited into the posterior
urethra by peristaltic action
• contraction of the urethral sphincter to prevent retrograde
passage of semen into the bladder
• propulsion of the seminal bolus into the penile urethra
• expulsion from the urethral meatus.
The first three are essentially sympathetic and are mainly medi-
ated by noradrenaline acting on α1-adrenoceptors in smooth
muscle. The fourth is dependent on somatic innervation (puden-
dal nerve) and involves rhythmic contractions of the bulbocaver-
nosus and other pelvic striated muscles.
Following ejaculation in the male there is a post-ejaculatory
refractory time (PERT) during which a second erection/ejaculation
PSYCHIATRY 6:3
is impossible. There is considerable interpersonal variability in the
PERT duration, but generally it increases with age. PERT probably
serves to ensure that each ejaculate contains adequate spermato-
zoa. PERT does not normally occur in women, who, therefore,
have the potential for multiple, serial orgasms within one sexual
scenario. It has not been established whether those women who
express a female ejaculation experience a PERT like men.
Orgasm
Orgasm is the tantalisingly brief ecstatic pleasure of the sexual
climax lasting from 5 to 60 seconds. They can occur without
having to be awake as they are experienced in sleep both in men
(‘wet dreams’) and women.
In the male, orgasm is usually, although not invariably, tem-
porally related to emission/ejaculation. Initially, there is the sen-
sation, caused by increased tension in the wall of the prostatic
urethra at the end of emission. This feeling, known as ejaculatory
inevitability, signals the end of any voluntary control over the
timing of ejaculation. A ‘pumping’ feeling arises from the rhyth-
mic contractions of the striated pelvic musculature propelling
the semen through, and forcefully expelling it from, the penile
urethra. Most males groan or vocalize involuntarily at each con-
traction.19 Finally, there is the post-orgasmic feeling of relief and
calm as the tensions developed during arousal are dissipated.
In women, orgasm is initiated with a transient sensation of
‘suspension’ or ‘stoppage’ and then a thrust of intense clitoral
sensual awareness that radiates out into the pelvis. This is fol-
lowed by a suffusion of warmth felt first in the pelvic area which
then spreads to the rest of the body. Finally, intense pleasure
sensations are concomitant with rhythmic clonic contractions
of the pelvic muscles. Uterine and anal contractions also occur.
Involuntarily groans or vocalizations are often present at each
orgasmic contraction and a post-orgasmic feeling of calm and
satisfaction from the dissipation of their sexual tension expe-
rience.19 Controversy still exists in relation to the typology of
women’s orgasms, namely those induced by clitoral or by vagi-
nal stimulation, as claims are made that they are subjectively felt
as different. There is now limited physiological evidence that the
pelvic/genital muscular contractions are different.7
Hormones and human sexuality
An account of the role of hormones in human sexuality is too
complex to be dealt with in this contribution but their impor-
tance should not be overlooked. Briefly, the sex steroids, espe-
cially androgens and oestrogens, have essential developmental
(organisational), maintenance and activational functions in both
males and females. Oestrogens are more involved in female sexu-
ality, especially the development and maintenance of genitalia
and breasts. Androgens, however, are important in both male
and female sexual arousability and libido, while the physiologi-
cal roles of the peptide hormones secreted at orgasm (prolactin,
oxytocin and vasopressin) are still uncertain.20
Conclusion
Sexual functioning involves an integrated series of physiologi-
cal processes with complicated peripheral and central control
systems. Our understanding of the physiology of the peripheral
93 © 2007 Elsevier Ltd. All rights reserved.
 Introduction
events in the male is advanced and we are now beginning to
elucidate those of the female. Much of our knowledge of central
mechanisms is derived from animal studies, and with current
advances in imaging technology it is becoming possible to assess
the relevance of findings in animals to the human state. A better
understanding of the central mechanisms involved in the control
of sexual functioning should identify new pharmacotherapeutic
approaches to sexual dysfunction. ◆
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Further reading
Andersson KE. Neurophysiology/pharmacology of erection. Int J Impot
Res 2001; 13(suppl 3): S8–17.
Goldstein I, Meston CM, Davis SR, Traish AM, eds. Women’s sexual
function and dysfunction – study, diagnosis and treatment. London:
Taylor and Francis, 2006.
Guiliano F, Rampin O, Allard J. Neurophysiology and pharmacology of
female sexual response. J Sex Marital Ther 2002; 28(suppl):
101–21.
Komisaruk BR, Beyer-Flores C, Whipple B. The science of orgasm.
Baltimore, MD: The Johns Hopkins University Press, 2006.
Lue TF, Basson R, Rosen R, Giuliano F, Khoury S, Montorsi F, eds.
Sexual medicine sexual dysfunctions in men and women. Paris:
Health Publications, 2004.
Meisel R, Sachs B. The physiology of male sexual behaviour. In: Knobil
E, Neill J, eds. Physiology of reproduction. New York: Raven, 1994.
94 © 2007 Elsevier Ltd. All rights reserved.