· To define amenorrhoea-oligomenorrhoea, dyspareunia, gynaecomastia, hypogonadism,
impotence, infertility, menarche, menopause, menstruation and phases of the
menstrual cycle, oligospermia-azoospermia, sterility, and virilization.
· To describe anticonception, anovulatory cycles, bleeding disturbances, castration,
cryptorchism, postmenopausal hormonal alterations, puberty, anabolic steroids
and doping, genetic and psychosocial sexual disorders.
· To explain the effect of anabolic steroids, the normal menstrual cycle, conception,
implantation, pregnancy, pregnancy tests, birth and suckling. To explain the
normal ovarian and testicular function, gametogenesis, erection, ejaculation
and sexual satisfaction (orgasm). To explain the effect of androgen-binding
protein, inhibin, aromatase, and the biosynthesis of steroids.
· To use the above concepts in problem solving and case histories.
gonads are concerned with the well being and preservation of the human race.
sperm decides the genetic sex (genotype). The Y chromosome is a constant
determinant of maleness.
differentiation of the genital ducts and of the external genitalia requires
foetal gonadal hormones. The foetal genital tract will always develop into
female genitals, if unexposed to embryonic testicular secretion.
· Amenorrhoea-oligomenorrhoea are terms used for absence - irregular,
infrequent menstrual periods. These signs suggest female
hypogonadism, when pregnancy is excluded.
· Azoospermia describes absence lack of sperm in the ejaculate
· Dyspareunia refers to female pain or discomfort during intercourse.
· Gametogenesis is the formation of ova and sperm. The primitive germ cells are divided by meiosis,
so the number of chromosomes is halved (22 autosomes and one sex chromosome).
sex is determined by the presence or absence of
the Y chromosome. The Y chromosome determines the development of testes and
maleness. The Y chromosome contains a sex
determining region (the SRY gene), which encode the testis
determining factor (TDF).
sex is the phenotypic sex (apparent female or apparent male).
sex is determined by the presence of normal ovaries or testes.
· Gynaecomastia refers to the occurrence of female breasts in
males. The causes are HCG-producing tumours, oestrogens or oestrogenic drugs.
· Hypogonadism (male) refers to a condition with small, soft
testes producing little sperm and testosterone. The condition is usually found
· Impotence is inability of the male to produce an adequate erection for satisfactory
· Infertility (subfertility) is a diagnosis used on a couple,
which has been unable to conceive during one year of unprotected intercourse.
The causes are oligospermia, tubule blockage, ovulatory disorders, or combined
problems with both persons in the couple.
· Menarche refers to the age at the first menstrual period.
· Menopause refers to cessation of periods, which usually occurs around the age of 50
· Menstruation is the onset of spontaneous regular uterine bleeding.
· Oligospermia refers to reduced numbers of sperm in the ejaculate. The causes are primary
testicular disease or blockage of the vas deferens.
· Puberty is the transition period from a non-reproductive to a reproductive state.
· Sterility refers to individual infertility. Chemotherapy
and other drugs may cause sterility. Surgical blockage of the tuba or the vas
deferens results in sterility.
· Virilization is the occurrence of male secondary sex characteristics in the female.
of other genetic concepts are given in Chapter
This paragraph deals with 1.
The sexual drive , 2. Sex before birth, 3. The menstrual cycle, 4.
Ovulation/Female orgasm, 5.
Conception, 6. Breast development, 7.
Labour, 8. Efferent activity
during coitus, 9. Sex hormones, and 10.
The sexual drive
We feel the sexual drive or desire
for sex (libido), when sex-related
areas in the higher brain centres are stimulated. These centres include
the limbic system, Stria terminalis and the preoptic region of the
hypothalamus. The desire for sex is increased by androgens in both sexes.
The sex desire of females is variable - for
some it increases near the time of ovulation, when oestradiol secretion is increasing, while others experience a peak
drive near menstruation. The CNS cells involved (see above) must contain sex
hormone receptors. Sex hormones are steroids. They are lipid soluble and
pass the cell membrane easily. After binding to cytoplasmic
receptors (the steroid-thyroid family), the receptor-hormone complex
translocates to the cell nucleus. Here the information is transcribed and
translated. The result is release of new proteins with the same information
into the cytosol, where the physiologic response is triggered. Castration is assumed to reduce female libido minimally, but male libido is most
often lost. Removal of one testis need not change the male libido. These
clinical observations reflect psychosocial differences, and not necessarily a
different libido mechanism in the two sexes. Hypothyroid persons lose their
sex drive. The sex desire (libido) is stimulated by a multitude of sense impressions (visual, auditive, olfactory, and
psychological). Potency refers to
the ability to engage in intercourse.
The brain is an important sex organ. Obviously, any natural body
contact can be considered part of a healthy sex life - including the
penetration of the penis in the vagina.
satisfaction is synonymous with orgasm in Western cultures. Orgasm is
the psychological climax or the culmination of total
commitment in a sexual act that is accompanied by a series of
physiologic reactions. Female orgasm involves spinal cord reflexes similar
to those involved in male ejaculation (see later). One very important reaction
is ovulation, which is an automatic consequence of copulation among many
animal species and periodically in humans.
Sexual enjoyment covers several phenomena.
For example the fetishist satisfaction of
wearing the clothes of the opposite sex. This is the important part of a
transvestites sex life. Some transvestites become asexual in the general
sense of the term, since they do not need partners. Some individuals prefer masturbation (onany) as a substitute for partnership. Many individuals prefer
heterosexual contacts; others prefer homosexual activities, while bisexuals
may prefer either sex - depending on the circumstances. Sexual activities can
vary. Besides, homosexual activity, oral sex, anal sex and many other variants
are not uncommon.
Sex before birth
Normal sexual development in the embryo
involves several processes. The sperm, which can be an X or an Y chromosome
sperm, decides the genetic sex or
sex genotype (Fig. 29-1). The genetic sex is independent of the ovum.
If the ovum is fertilised by an X
spermatozoa (22 + X-chromosomes) the offspring is XX, a female. If the ovum
fertilises by an Y spermatozoa (22 + Y-chromosomes) the offspring is XY, a
male (Fig. 29-1).
29-1: The sperm decides the genetic sex. The presence of the Y chromosome
is the determinant of maleness.
Sex differentiation in the embryo usually
harmonises with the sex genotype,
but hormonal disturbances can lead to abnormalities. Proliferation of
non-germinal and germinal cells in the genital
ridge creates the gonadal primordia,
which develops into a cortex surrounding the medulla. Until the 7th week of
gestation, each sex has a bipotential system (the sexual indifferent stage)
with both Wolffian and Müllerian ducts. The urogenital
sinus develops into the external genitals in both females and males.
Around the 7th week, the medulla of the
primitive gonad begins to differentiate into a testis, if an Y chromosome is
present. This is because the Y chromosome contains the so-called SRY
gene (the sex determining region of Y), which encodes the testis-determining
As the testes grow and their Leydig cells
start to produce testosterone, the Wolffian
ducts develop into the male reproductive tract (epididymis, vas deferens,
seminal vesicles and the ejaculatory ducts), whereas the Müllerian ducts regress. Testosterone stimulates the growth and
differentiation of the Wolffian ducts in the male. The regression of the
Müllerian ducts is caused by the antimüllerian
hormone from the Sertoli cells.
Conversely, in the female, the cortex of the
indifferent gonads differentiate into ovaries,
if only two X chromosomes are
present and no Y. In the female foetus, where there is a developing ovary and
no antimüllerian hormone, the Müllerian ducts develop into the female
reproductive tract (the uterine tubes, uterus and the upper vagina), and the
Wolffian ducts degenerate because the ovary does not secrete testosterone.-
When a normal female foetus is exposed to androgens during the period of
differentiation of the external genitalia, an apparent
male can result.
Visible differentiation of the gross anatomy
does not appear until late in the second month of embryonic life. Testosterone
causes the differentiation of the
foetus to a male. The foetal genital tract will always develop into female
genitals, if unexposed to embryonic testicular secretion. The genital
sex is a phenotypic female. If testosterone is present, male external sex
organs develop and the genital tubercle elongates to form the male phallos. If testosterone is absent, female organs
develop instead. It is the action of testosterone and 5-a-dihydrotestosterone on the urogenital sinus that is behind the
normal development of the male external genitalia. In the last months of
gestation the growth of the external genitalia depends upon foetal pituitary
One population of cells in the indifferent
gonade develops into the granulosa cells of the ovarian follicle and the
Sertoli cells of the testicular seminiferous tubules. These cells support and
mature the germ cells. – Another population of so-called interstitial cells develop into the theca cells of the ovary and the
Leydig interstitial cells in the testis. The Leydig interstitial cells secrete
testosterone, in response to human
chorionic gonadotropin (hCG) from the placenta.
The presence of normal ovaries or testes
determines the gonadal sex. Without
normal ovaries or testes any genetic sex will develop into an apparent female.
Foetal plasma growth hormone (GH) concentrations are high, but GH-receptors are
deficient and foetal GH is not essential for linear growth. Prolactin and
placental GH act as growth factors and induce the presence of IGF-1 and IGF-2.
A small transfer of maternal thyroid hormone is important for early foetal
development. At birth, the babys own thyroid hormone is important for CNS
development and somatic growth. Foetal PTH stimulates the Ca2+-transfer
across the placenta and controls plasma-Ca2+. Foetal ACTH is
important late during gestation in particular at birth, and the cortisol
concentration is high in umbilical cord plasma. Foetal pancreatic a-and b-cells
are functional by 14 weeks of gestation, but their release of glucagon and
insulin is low.
In 1949 Barr et al. found a densely coloured
body in the periphery of the nucleus (the Barr
body or sex chromatin) of the
buccal mucosa of females. The Barr body is also present in other individuals
with two or more X-chromosomes in each cell. Individuals with one sex
chromatin (Barr body) also have a drumstick attached to a small fraction of their leukocytes (Fig.
29-6). We find sex
chromatin and drum sticks in cells, whether they divide or not. Chromosomes
are only visible in dividing cells. The maximum number of sex chromatin and
drumsticks is always one less than the number of X-chromosomes (Fig. 29-6).
The menstrual cycle
The menarche is the age at the first menstrual
bleeding. It often occurs
between the 12th and the 14th year.
LH and FSH are coordinators of gonadal
function. The secretion of these pituitary gonadotropins is regulated through
negative feedback by the plasma concentration of gonadal steroids. LH
stimulates the interstitial cells of the ovaries (and testes), but LH also
acts on female granulosa cells. LH binds to a LH-receptor, which spans the
cell membrane several times. The LH receptor acts via adenylcyclase and with
cAMP as a second messenger. Prostaglandins may increase the cAMP effects.
Maintained stimulation by LH down-regulates the number of LH-receptors on the
surface of gonadal cells.
FSH acts on ovarian granulosa cells (and
testicular Sertoli cells) by binding to FSH-receptors, partially homologue
with the LH-receptors. The increase in cAMP following FSH-receptor binding transcribes the aromatase gene and stimulates oestrogen synthesis. FSH stimulates
synthesis of inhibin and peptide/protein products from granulosa and Sertoli
cells. FSH amplifies the sensitivity to LH by increasing the number of
LH-receptors on granulosa cells.
LH and FSH increase glucose oxidation,
lactic acid production and protein synthesis.
The menstrual cycle starts at the first day of bleeding (menstruation).
The bleeding is due to decrease of oestrogen and progesterone secretion. The
FSH and LH secretion start to rise and stimulate the growth of several
follicles ‑ in particular following the bleeding. One of these – the
dominant follicle – select itself by outstripping the others and grow so
fast that the follicle can protrude more than 10 mm from the surface of the
ovary. The dominant follicle has an increased oestrogen synthesis due to
increased aromatase activity. Oestrogen from the granulosa cells of the
dominant follicle binds to specific, cytoplasmic
receptors (of the steroid-thyroid-family) in the endometrial and other
uterine cells. Oestradiol activates and stimulates formation of oestrogen and progesterone receptors.
29-2: The menstrual cycle in a female.
Oestrogen increases the thickness of the endometrium, the size of the myometrial cells and the number of gap junctions thus allowing the myometrium to work as a
unit. The oestrogen phase is also called the proliferative phase. The concentration of sex hormones in plasma is
shown in Fig. 29-2. Oestrogens work synergistically with progesterone to
release gonadotropins by positive
feedback just before ovulation.
Following the rupture of the follicle (ovulation),
the corpus luteum produces increasing amounts of progesterone in
addition to oestradiol also from a new developing follicle (Fig.
Due to the priming effect of oestrogen on progesterone receptors, both hormones
stimulate the growth of the endometrial glands, so that they curl like a
helix. The progesterone effect in particular provides the
endometrial/myometrial tissues with their high
secretion and bloodflow, so the
uterus is prepared to receive the fertilised ovum. During sexual stimulation
the vaginal fluid secretion increases, as does the bloodflow of the organs
If fertilisation does not occur, the level
of oestradiol and progesterone switches off both gonadotropins. The corpus
luteum fades out and degenerates with no LH to support it (Fig.
The ovarian hormones almost cease to flow,
and the uterus is deprived of their stimulating action. Therefore the uterus
shrinks and sheds its swollen lining.
On the first day of the menstrual bleeding,
the low progesterone and high
prostaglandin level probably releases enough Ca2+ to start spontaneous contractions of the myometrial cells.
Ca2+ -ions enter myometrial cells and stimulate their activity in
the secretory (progesterone) phase.
The gap junctions synchronise these
contractions, so that they include the whole myometrium. This can make
excretion of blood and necrotic cells (containing prostaglandins) extremely
painful. Prostaglandins dominate in menstrual fluid and stimulate the
spontaneous activity of the human myometrial cells. A normal bleeding corresponds to a loss of up to 50 ml of whole blood. The mixture of vaginal fluid and
menstrual blood produces a pH close to that of normal blood. The average cycle
length is 28 days.
ADH (vasopressin) secretion from the
neurohypophysis can cause pre-menstrual
tension and an unpleasant increase in body fluid volume.
sudden increase in the plasma level of oestradiol maintained for more than 24
hours can increase FSH output by positive
feedback. This is called the positive
feedback release ovulation. The pulsatile release of GnRH from the
hypothalamus is possibly stimulated by the high oestradiol concentrations in
mid-cycle and oestradiol increase the number of GnRH receptors on the
gonadotropic cells of the anterior pituitary. A neural hypothalamic pulse
generator has been proposed to be involved in ovulation, and in some cases
female orgasm triggers ovulation.
At lower plasma levels oestradiol is a
potent inhibitor of GnRH secretion and thus of FSH and LH output (negative feedback). The negative feedback forms the basis for the
ovulation-inhibition by contraceptives.
LH binds to a membrane LH-receptor and acts
via a G-protein, adenylyl cyclase and cAMP. LH mobilises cholesterol and its
conversion to progesterone.
FSH acts on ovarian granulosa cells and
testicular Sertoli cells by binding to a membrane receptor homologous with the
LH-receptor. The binding increases the transcription of the aromatase gene,
the oestrogen and the inhibin synthesis.
The primary inhibitor of FSH secretion is
the peptide, inhibin, that is
secreted by the ovary (and testis), and blocks the effect of GnRH.
The oestradiol release from the dominant
follicle increases sharply in the last part of the follicular phase. This
triggers the preovulatory surge of
gonadotropins (LH and FSH).
LH surge induces an enzyme that increases the synthesis of leukotrienes,
prostaglandins and thromboxanes. These molecules create an inflammation that
causes rupture of the follicle. LH continues to act on the follicular
granulosa cells, turning them into a yellow endocrine organ, the corpus luteum.
The time for preplay including clitoral
and multifocal stimulation is important for most females. A clitoral
orgasm in the preplay often triggers more female orgasms later during the
intercourse. Female orgasm is released from the spinal cord reflexes via
sympathetic signals in the pudendal nerves.
Two persons with a simultaneous sexual drive
must have the necessary time for the sexual act. If they are also in love, it
is natural to explore and use all means to satisfy each other.
Years ago, when the Kinsey report was made,
the average duration of sexual intercourse was measured in seconds in the US.
American males able to ejaculate even faster were assumed to be particularly
virile. Today, such a short performance is considered a male disease called premature
Conception and pregnancy
100-200 million sperms are produced each day of the fertile lifespan. The
female foetus may contain 6
million oocytes, but the number decreases throughout her life (less than half
a million at puberty and she may have 500 ovulations before the menopause).
moving spermatozoa passes through the uterus while prostaglandins inhibit
their spontaneous activity. The spermatozoa can keep their vitality for more than 2 days,
if they reach the fallopian tube. They lose their protective cover in the
fallopian tube. The head of the spermatozoa swell and liberates proteolytic enzymes.
These enzymes can dissolve the zona pellucida around the egg (oocyte). All
these events in the spermatozoa takes days before it meets with the oocyte.
The oocyte can only live 12-24
hours without conception.
sperms bind to the zona pellucida, but only one penetrates the wall – and
blocks the entry of other sperms. Fusion of the two sex cell membranes forms
the zygote, and the mitosis is complete within 24 hours.
The zygote passes into the uterine tube
within a few days, protected against other spermatozoa by an increased
permeability for K+, so that the zygote membrane hyperpolarises. Peristaltic
movements of the tube and ciliary motion conduct the zygote to the uterine
cavity while undergoing cleavage
division. Each cell is capable of developing into a complete human being
up to the eight-cell stage.
At the morula
stage, the cells start to develop into the inner cell mass or blastocyst, and the trophoectoderm or trophoblast. Seven days after conception, the blastocyst loses the zona pellucida and implants in the wall of the uterus (nidation).
Nidation depends on prior conditioning of the endometrial stromal cells by
progesterone bringing it into the proliferative phase. The stromal cells
accumulate nutrients and swell or decidualize around the blastocyst. Endometrial laminin and fibronectin facilitate
adhesion. Histamine and prostaglandins increase the permeability of the vessels around the nidation site. More
than 2/3 of all conceptions result in miscarriage, because of insufficient
attachment or other anomalies.
trophoblast, which give rise to the extra-embryonic
tissues differentiates into two
cell types. An inner layer of cytotrophoblasts,
and an outer layer of syncytiotrophoblasts.
The cytotrophoblasts synthesise stimulatory hormones such as CRH, GnRH, TRH
The syncytiotrophoblasts synthesise first of
all human chorionic gonadotropin (hCG). The b-group of hCG is specific and detected in maternal
plasma 6 days following conception by specific antibody methods. The hCG is
detectable in the urine within 9 days after conception.
The placenta is a fantastic hormone factory,
which produces large amounts of hCG, relaxin. oestradiol, progesterone and
human chorionic somatomammotropin (hCS or human placental lactogen, hPL). The
hPL is synthesised from the 4. week of gestation. The hPL stimulates maternal
lipolysis and inhibits insulin effects, causing hyperglycaemia.
The hCG is chemically related to TSH, FSH
and LH. The hCG acts like LH and binds to the LH-receptors. The secretion of
hCG is stimulated by GnRH produced by cytotrophoblasts. This is what keeps corpus
luteum in being, and the pregnancy continues.
During pregnancy, hCG thus conserves the corpus
luteum, taking over the role of LH.
The secretion of hCG stimulates ovarian release of progesterone and
oestrogens just like LH. The hCG stimulates production of relaxin, inhibits
the maternal secretion of LH and stimulates the maternal thyroid gland causing
struma or hyperthyroidism in some pregnant females. Inhibin A from foetal
trophoblasts peaks within the first week and suppresses maternal FSH
secretion. Inhibin B concentrations remain low throughout gestation. LH and
FSH concentrations in foetal plasma peak in mid gestation.
29-3: Variations in plasma hormone concentrations during a normal
pregnancy (42 weeks).
The plasma [hCG] reaches a peak value after 10
weeks of pregnancy, when the syncytiotrophoblast count is maximum (Fig.
29-3). - Shortly after delivery hCG disappears.
The first peak on the plasma progesterone
curve is progesterone produced by corpus luteum. The placenta takes over the
progesterone production during the remaining pregnancy period ending with a
peak concentration before birth. Progesterone protects the foetus in the
uterine cavity by stimulation of endometrial glands that nourish the zygote
and by maintenance of the decidual cells. Progesterone inhibits uterine
contractions (inhibits prostaglandin synthesis and oxytocin sensitivity).
and the placenta form a foetoplacental unit. It produces all the hormones
necessary for a successful pregnancy. Steroid precursors are delivered from
both the foetus and the mother. Oestrogen (oestradiol, oestrone, and oestriol) concentrations rise steadily throughout pregnancy (Fig. 29-3).
Oestrogens stimulate the growth of the myometrium and of the ductal system of
the breast. Oestriol production independs on the foetal adrenal cortex, so
maternal plasma oestriol provides an estimate of the foetal condition.
The placental progesterone blocks the
menstrual cycle of the mother. Pregnant females therefore develop amenorrhoea.
During puberty FSH, LH, growth hormone, and
insulin are important for the breast development. The thyroid hormones (T3/T4)
are permissive. Before puberty,
plasma LH and FSH concentrations are low. There is no reaction to the low
concentrations of gonadal steroids and inhibin.
Oestrogens are growth factors for the
myometrium and for the ductal system og the breast during pregnancy. At the
end of pregnancy there are other hormonal events. Progesterone secretion
reaches a peak and then falls. This fall in progesterone allows the pituitary
to release prolactin (LTH).
Prolactin from the maternal pituitary rises
throughout pregnancy. Prolactin acts on the enlarged mammary glands turning
them into milk producers. Prolactin
develops the milk producing acini in the breasts during pregnancy. Prolactin
Inhibiting Factor (PIF or dopamine) from the brain inhibits the prolactin secretion.
The baby’s suckling stimulate the
secretion of prolactin and oxytocin, but oestradiol and sexual stimulation is
also involved. The mechanical stimulation of the breast increases the
secretion of prolactin from the pituitary, but the response is strikingly
reduced by alcohol.
Prolactin is important for the development
of the mammary gland tissue,
oxytocin, however, governs the ejection
of milk during lactation. Oxytocin causes contraction of the myoepithelial cells in the milk ducts (just as it
does in the myometrial cells).
Mother-milk contains long chain fatty acids
that are essential for brain development. Suckling babies are protected
against juvenile diabetes in comparison to non-suckling babies. Cow's milk
contains much more protein and less lactose than human milk.
When the foetus has reached a critical
size, the myometrial fibres are stretched, which increase their
At the end of pregnancy
the uterus is sensitised by oestrogen.
After a high peak in progesterone secretion the progesterone output falls.
This fall in progesterone allows the uterus to respond to oxytocin, whose release is the final trigger for
The foetal pituitary-adrenal axis signals to
the placenta a decrease in the progesterone-oestrogen
ratio acting on the myometrium. This increases myometrial contractions
that are mediated by prostaglandins (PGE2 and PGE2-a).
A local increase in prostaglandin concentration increases myometrial cell Ca2+ and triggers uterine contractions. The density of oxytocin receptors in the
myometrium increases throughout gestation and particular at term.
The role of the stable plasma concentration
of maternal oxytocin at parturition
is an enigma. Oxytocin is released according to a pulsatile pattern. The
frequency of oxytocin pulsations increases at labour. This fact does not
exclude an important role of oxytocin in normal human parturition.
Therapeutic doses of oxytocin initiate
labour in most cases at the end of gestation,
The foetal cortisol production prepares the
foetus to adapt to extrauterine life by stimulating lung maturation, by
increasing the hepatic glycogen stores, and by promoting closure of the ductus
arteriosus (Fig. 12-7).
Relaxin is an insulin-like polypeptide produced by the corpus luteum and placenta. The
hormone relaxes pelvic articulations, suppresses myometrial contractions and
softens the uterine cervix in order to facilitate passage of the foetus.
Several other factors are involved in human
labour, but the exact trigger mechanism remains unclear.
Efferent activity during coitus
The activity in males is described as an
example. The typical sequence of efferent events in the male includes
erection, emission of semen and ejaculation.
Erection means penile rigidity and elongation due to
parasympathetic vasodilatation. Psychological factors trigger penile rigidity,
and sexual thoughts can cause erection, emission and ejaculation. The penis
contains erectile tissue located in two dorsal corpora cavernosa and in a single ventral corpus spongiosum. All the cavernous spaces of the three penile
corpora receive blood from thick-walled arteries ending centrally in each
corpus. The blood leaves the cavernous spaces through thin-walled veins
starting peripherally. Tactile stimuli, especially from the very sensitive glans
penis activate sensory, somatic fibres in the pudendal nerve, whereby
impulses reach the sacral plexus. Parasympathetic impulses (S2-S4)
from the sacral plexus elicit dilatation of the arteries and constriction of
the veins in penis. The cavernous spaces are hereby filled with blood under
high (arterial) pressure within seconds, causing the penis to become hard and
elongated for penetration. - Erection occurs quite normally during the REM
phases of sleep.
Emission is caused by sympathetic contraction of smooth muscles (in epididymis, ducts
and glands), which drive the fluids into the posterior urethra. Oxytocin
ejects sperm into semen. Two exocrine glands near the neck of the bladder (the
seminal vesicles and the prostate) secrete fluids that nourish the sperm and
transport it through the urethra during the sexual act. The prostate gland
supply an alkaline secretion containing Ca2+, Zn, and phosphatase
to the ejaculate. The seminal vesicles supply fructose and prostaglandins.
These two secretions neutralise the acid semen and help propel the spermatozoa
towards the ovum. Seminal fluid also contains gonadotropins, sex hormones,
inhibins, endorphins, relaxin, proteases and plasminogen activator. Epididymis
supply sperm-coating proteins.
Ejaculation: Ejaculation is a sympathetic response. Contractions of skeletal muscles expel
the semen from the urethra in a rhythmic
pattern. Signals from glans penis reach the lumbar region of the spinal cord
through afferent fibres in the internal pudendal nerves. Filling the posterior
urethra with semen triggers sensory impulses that travel through the pudendal
nerves to the spinal cord. The spinal cord transmits rhythmic signals to the skeletal
ejaculation muscles (the ischio-and bulbo‑cavernous muscles and
those of the pelvis). These rhythmic signals stimulate rhythmic contractions
that expel the semen from the urethral meatus into the female genitals. – A
typical ejaculate contains 300 million spermatozoa in 3 ml.
Inside the female
genitalia the sperm is subject to the process of capacitation, which takes place within 6 hours. The sperm head is coated with substances
from the ejaculate, Ca2+ enters the sperm, sperm motility
increases, and the ability to penetrate the ovum is enhanced. The acrosomal
membrane fuse with the outer sperm membrane, so that pores are formed and
proteolytic enzymes can reach the surface of the sperm head.
oestrogens, progesterone, androgens and eichosanoids. Steroid synthesis in the
gonads begins with cholesterol from acetyl Coenzyme A, and is almost identical
to that of the adrenal cortex.
Oestrogens stimulate the female genitals and act to produce
female secondary sex characteristics when a female enters puberty. Oestrogens
and progesterone all enters the cell cytosol easily and bind to cytoplasmic
receptors of the steroid-thyroid family. Oestradiol increases the synthesis of oestrogen- and progesterone-receptors.
These sex characteristics include the
progressive growth of fallopian tubes, uterus, vagina, and external genitalia;
also the fat deposition in breasts, buttocks, and thighs (Fig.
ductal and stromal growth of the breasts is initiated just as the general
growth at puberty with increased RNA and protein synthesis in the body cells.
Oestrogens stimulate secretion of prolactin from the pituitary lactotrophic
cells, increase the thickness of the endometrium and the size of the
myometrial cell and their number of gap
junctions. Oestrogens stimulate the hepatic production of essential
proteins (eg, TBG, blood clotting factors, plasminogen, and HDL), but they
inhibit formation of antithrombin III and LDL. Retention of salt and water can
Oestrogens consist of oestradiol, the principal ovarian oestrogen, oestriol, the major placental oestrogen, and oestrone, an important ovarian and postmenopausal hormone.
At a certain level oestradiol increases GnRH
secretion and FSH output by positive feedback. There is also an increased LH
sensitivity to GnRH. This feedback is already called positive feedback release ovulation, where the leading follicle
ruptures. At lower oestrogen levels in the blood, it is a potent
inhibitor of gonadotropin releasing hormone (GnRH) secretion and thus of FSH
output. This is the reason for the ovulation-inhibition by many oral contraceptives. In the blood oestradiol is bound to sex
29-4: Feedback loops and targets organs in the
The hypothalamic GnRH secretion shows a
cyclic variation in adult females of approximately 28 days, probably a genetic
code imposed by the CNS.
1. Peaks of GnRH
release reach the adenohypophysis through the portal system, and release
both FSH and LH to reach the ovary via the systemic circulation (Fig. 29-4).
2. FSH stimulates follicular growth, inhibin-release from stromal cells, and aromatase activity in the ovary. Aromatase converts ovarian and other androgens to oestrogens.
3. LH stimulates the ovarian androgen production.
4. Inhibin is the primary inhibitor of FSH
release by blocking the effects of GnRH on the adenohypophysis.
Oestrogens are responsible for the female
secondary sex characteristics, the maintenance of libido, anabolic effects,
and the negative feedback on the GnRH secretion and the Gonadotropin secretion
of the adenohypophysis (Fig. 29-4).
Progesterone secretion rises sharply in the luteal phase of
the menstrual cycle, and modulates the effect on oestrogens on the endometrium
and the myometrial cells. Since the oestrogens have primed all the
progesterone receptors, both hormones stimulate the growth of endometrial
glands so they curl. Progesterone stimulates the secretion and high bloodflow
of the uterus, so it is prepared to receive the fertilised ovum. Progesterone increases the basal core temperature by 0.5 oC,
which is used as an indicator of ovulation.
the absence of pregnancy, progesterone secretion falls and switches off the
release of GnRH and both Gonadotropins (Fig. 29-4). The corpus luteum
degenerates, resulting is sloughing of the endometrium (ie, menstruation).
Pregnancy is maintained by progesterone, and
uterine contractions are inhibited. Progesterone has a certain aldosterone
effect by competition for the same receptors. Progesterone has a negative
effect on the lipid profile by increasing the LDL and reducing the HDL
fractions in the blood plasma.
Androgens, such as testosterone, are anabolic, maintains spermatogenesis and libido, and
act to produce male secondary sex characteristics. These characteristics are
the deepening of the voice at puberty, beard, body hair, sebaceous glands in
the skin, as well as the growth of the skeleton, the striated muscle system,
the external genitalia and male behaviour-attitude. The primary sex structures
are the testes with seminiferous tubules, epididymis, prostate, and seminal
vesicles. Testosterone is responsible for the growth, maturation, and
maintenance of the primary sex structures. Androgens stimulate the growth and
polyamine synthesis in the prostate and the seminal vesicles. Hereby RNA
synthesis is stimulated and the result is often hypertrophia and hyperplasia.
Testosterone increases LDL and decreases HDL concentrations in plasma.
29-5: The feedback system of the hypothalamic-pituitary- testicular axis.
Testosterone is reduced to two other potent androgens
in many tissues. Testosterone is thus a prohormone for these potent androgens.
Most of the testosterone in plasma binds to sex
steroid-binding globulin, a small fraction binds to albumin and only 1% is
free testosterone. Thyroid hormone and oestrogens increase the concentration
of sex steroid-binding globulin and thus reduces the free fraction. Androgens
have the opposite effect. Testosterone diffuses easily into the cell cytoplasm
and binds to a cytoplasmic receptor belonging to the steroid-thyroid receptor
male sexual system is controlled in the
1. GnRH (= LHRH) is released from hypothalamic
cells in a pulsate pattern, and stimulates release of LH and FSH from
gonadotropic cells of the adenohypophysis (Fig. 29-5).
2. LH stimulates the Leydig cells of the testes
to produce testosterone. These cell also produce small amounts of oestrogens,
oxytocin and subunits of pro-opio-melanocortin.
3. FSH and testosterone stimulate the Sertoli
cells of the testicular seminiferous tubules to produce spermatocytes and
4. Inhibin is a glycoprotein that reduces the pituitary FSH secretion (blocks the effects
of GnRH) by negative feedback (Fig. 29-5). Activins are synthesized by subunits of inhibin. The Sertoli
cells produce inhibin, as do the
granulosa cells in females. Inhibin inhibits FSH but not LH secretion by the
pituitary gland. Activin stimulates FSH secretion just as GnRH. Follistatin
binds and neutralises activin, so follistatin inhibits FSH-secretion.
5. Testosterone is responsible for the male
secondary sex characteristics, the maintenance of libido, anabolic effects,
and the negative feedback on the GnRH secretion and the Gonadotropin secretion
of the adenohypophysis.
during puberty is due to testosterone, but in the female adrenocortical
androgens are involved. Testosterone promotes protein synthesis (anabolic
effect). Anabolic steroids have been synthesized, which have a powerful
anabolic action but only a modest androgenic action. These artificial hormones
are still used to produce short-term super-athletes.
Such a misuse of medicine for doping purposes often results in addiction,
which has serious psychological, social and physical effects.
hypophysis produces four sex-related hormones FSH, LH, prolactin and
oxytocin. LH is also called Interstitial
Cell Stimulating Hormone (ICSH) in the male, because it stimulates the
Leydig interstitial cells that produce testosterone, which in turn
specifically inhibits LH secretion. Removal of the male pituitary causes
complete loss of all testicular functions; administration of FSH and ICSH then
restores these functions completely.
Eicosanoids are oxygenated, unsaturated 20-carbon fatty
acids that originate primarily from arachidonic acid by activation of phospholipase A2. Eicosanoids exert important effects on
most human cells. Arachidonic acid is a major component of the phospholipids
of membranes. Arachidonic acid is
converted to prostaglandins and thromboxanes by cycloocygenases, to leucotrienes by three types of lipogenases, and to epoxides by cytochrome P-450-dependent mono-oxygenases.
Prostaglandins and thromboxane (TxA2)
are synthesized in response to stimuli, and they mainly act locally as autocrine or paracrine hormones. Prostaglandins (PG) are abbreviated PGD,
PGE, PGF, PGG, PGH, and PGI2 (prostacyclin). Leucotrienes (LT) are
abbreviated LTA, LTB, LTC, LTD,
LTE, and LTF. The leucotrienes LTC4 and LTD4 are
TxA2 is not only an activator of
platelet aggregation, but also an effective bronchoconstrictor, and TxA2 constricts both the cerebral and the coronary arteries.
Prostaglandin E2 (PGE2) can be used to induce labour just as oxytocin. PGE2 and PGF2a increase uterine contractility by Ca2+-influx
and moderation of cAMP. Prostaglandins are especially useful in
PGE is a potent vasodilatator, which can be
used for intracavernous injection for impotence.
Young children have low plasma
[gonadotropin] from birth. The gonadotropin releasing hormone is formed in the hypothalamus (a decapeptide GnRH = LHRH), and stimulates pituitary
gonadotropins to pulsate secretion of FSH and LH (= ICSH). Through
childhood they develop pulsate secretion of pituitary gonadotropins, with a LH
peak at night in puberty. The nocturnal LH peak disappears when adult status
At the onset of puberty a timing device in
the brain triggers the gonadotropin producing machinery in the hypothalamic-pituitary-testicular
axis. Puberty is probably triggered by GnRH in a sufficiently mature CNS.
The hypothalamic neurons mature in accordance with a genetic (familial)
Puberty is a maturation process descending
from the programmed brain (hypothalamus) to the pituitary gland, the gonads
and eventually to the entire body. Hormones are produced at high rates, and
the secondary sex characteristics then develop.
Negative feedback control operates both
before and after puberty, but the output of FSH and ICSH from the
adenohypophysis is more than 100 times greater in young adults than in boys.
Circulating inhibin is the primary inhibitor
of FSH secretion by negative feedback on the pituitary gonadotropins. FSH
stimulates Sertoli cells to produce more inhibin at puberty (Fig.
Circulating testosterone regulates ICSH
secretion by negative feedback primarily on the eminentia mediana hypothalami.
The plasma [testosterone] is highest during the night and in the morning
(circadian rhythm) but there is virtually no seasonal rhythm with testosterone
secretion in humans.
Enlargement of the testes is the first
clinical sign of male puberty. The testis consists of Leydig cells that
produce testosterone. Gap junctions connect adjacent Leydig cells, and their
testosterone has local nourishing effects on germ cells. The seminiferous
tubules contain the germ cells (spermatogonia) and Sertoli cells. Each
spermatogonium can divide into 64 spermatozoa within 65 days. The Sertoli
cells secrete a wide variety of growth factors, activin, inhibin, oestrogens
and an androgen-binding protein, all of which nourish the germ cells. The
seminiferous tubules drain into rete testis Halleri, which communicates with
the epididymis via ductuli efferentes. The epididymis is a maturation chamber
for spermatozoa, where they lose their cytosol and become increasingly mobile
within a few weeks. The store of mature spermatozoa is emitted into the female
genitalia during copulation. The human testes of an adult male are positioned
in the scrotum at a temperature around 35oC.
In disease or old age the seminiferous
tubules may cease functioning, but the sexual
capacities (other than fertility) are well maintained as long as
testosterone is produced.
Aberration of sex development can arise from
two different causes. 1. The sex chromosomes can create genetic sex disturbances,
hormones can disturb our sex
differentiation. This paragraph also deals with 3.
Psychosocial sex-deviations, 4. Cryptorchism, 5. Castration, 6.
Oral contraception, 7.
Impotence/Prostate disorders, 8.
Menstrual disorders/Occlusion of the fallopian tube, 9. Menopause, 10. Osteoporosis. 11.
Breast cancer, and 12. Abortion.
Sexually related infections are gathered at the end of Chapter
In 1938 Turner described a syndrome in small
persons, retarded in growth and in sexual development. They are apparent
females with small or no ovaries and a XO
chromosomal karyotype. Since they have only one sex chromosome (X), their
total chromosome number is 45. The Turner
patient lacks the inputs from two active X chromosomes and from an Y
chromosome. The lack of antimullerian hormone and testosterone leads to
Mullerian duct development and female genitals, but the ovary is just a
fibrous streak devoid of germ cells. The Turner patients have no sex chromatin
and no drum stick (Fig. 29-6).
In 1942 Klinefelter described a syndrome in persons appearing as men. These males are tall, have
small dysgenetic testes, some have female breasts (gynaecomastia), and they are sterile. Their cells contain XXY
chromosomes (47 instead of the normal 46). Thus Klinefelter patients must have
one sex chromatin and one drumstick just like normal females (Fig. 29-6).
These phenotypic XXY-males have
significantly higher LH & FSH, and lower blood [testosterone] than matched
XY controls. The seminiferous tubule development and spermatogenesis are
deficient in Klinefelter males. The XXY-males did not show more feminine
behaviour than matched controls. A similar group of tall males with XYY
chromosomes were not extraordinarily masculine. Some XYY-males have
significantly higher [testosterone] in their blood than matched XY controls.
Some small super women have an extra X chromosome: XXX, making a total of 47
chromosomes. We expected them to have two sex chromatin and two drumsticks,
and this has been confirmed. The XXX females have deficient germ cell
development and often a short reproductive life.
29-6: Intersex syndromes.
Apparent men with XXXY (48) chromosomes have
Klinefelter characteristics with
testes, and also two sex chromatin and two drumsticks (Fig. 29-6).
Individuals with four X-chromosomes are
extremely rare. They are apparent
females with XXXX (48), and apparent
males with XXXXY (49). Cells with 4 X-chromosomes contain a maximum of 3
sex chromatin (Barr bodies) and 3 drumsticks, regardless of whether the cells
come from apparent females or males (Fig. 29-6).
A very small number of individuals end up
being of indeterminate gonadal sex (ie,
has both ovarian and testicular tissues present). Some persons have an ovary
on one side and a testis on the other - a true
hermaphrodite. In the Greek
mythology Hermaphrodites was the
child of Hermes and the beautiful Aphrodite. Pseudo‑hermaphrodites have external genitals from both sexes,
but only one gonadal sex. Males have normal XY chromosomes, but small testes
with poor sperms (poor spermatogenesis). Some of these genetic (XY) boys are
born as apparent girls, but they may change from female to male at puberty if
the penis grows. An enzyme defect that blocks the conversion of testosterone
to 5-a-dihydrotestosterone disturbs the development of the external
genitals. Female hermaphrodites have ovaries, female ducts, XX chromosomes,
and varying degrees of masculine differentiation of the external genitals. Any
XY individual with a genetic defect in testosterone synthesis develops testes
due to the presence of the Y
chromosome, and Mullerian duct regression due to the presence of antimullerian
hormone. The Wolffian duct does not develop normally, because of the
Other XY individuals lack the androgen
receptor. They develop testes (Y chromosome presence) and the so-called X-linked
testicular feminisation syndrome. These XY persons show Mullerian duct
regression because the antimullerian hormone is present. The lack of androgen
receptors and the effects of androgens on the Wolffian ducts prevents
masculinization and the external genitals are feminine.
Hormonal differentiation disturbances
The virilising effect of testosterone on the urogenital sinus in early life
causes the adrenogenital syndrome in
XX individuals. They have ovaries (XX chromosome presence) and the Mullerian
duct develops normally, because of the absence of antimullerian hormone. The
androgen hypersecretion results in variable development of male external
genitalia. The adrenal hyperplasia is caused by enzyme defects.
XY individuals with deficient testosterone
synthesis ability to convert testosterone to dihydrotestosterone develop
testes, but the Wolffian duct structure are underdeveloped to a varying degree
ranging from a partial to a complete female pattern.
XY individuals who lack oestrogen receptors
or have a mutant gene for aromatase, lack oestrogen effects. The functional
lack of oestrogen results in unfused epiphyseal zones, so these males are
tall, and they have high plasma concentrations of LH although testosterone is
identity is the individual perception of herself or himself as a female or a male. Sex identity
is established early, and is not lost by castration. Both psychological and
social factors can interfere with normal sexual development on the
psychological plane. An imminent urge to change sex (operative sex shifts
etc.) characterises trans‑sexual
role is the social behaviour or
cultural role played by or forced upon each individual. Some male homosexuals
wish to express their femininity while other males clearly signal that they
are men. Transvestites love to dress
like the opposite sex. Transvestites are heterosexual, homosexual or asexual
just as others.
Cryptorchism means hidden orchids (testes). The flower orchid (French orchidé) has a
root, which is actually shaped like a testis.
If the testes do not descend from the
abdominal cavity to the scrotum, heat destroys the sperm-producing
seminiferous tubule cells. Heat does not harm the Leydig
(testosterone-producing) interstitial cells.
Certain cultures castrate boys to preserve
their tenor voices. Puberty and natural sex development does not take place.
Adult males retain their secondary sex characteristics and erection but they often lose libido. Eunuchs are more or less
trustworthy in Harems.
The effects of castration of adult females
are surprisingly trivial, as long as the pituitary is working well.
Castration, of course, stops their menstrual periodicity (artificial menopause), and they are sterile.
contraception is obtained with tablets (pills)
containing 20-30 mg
ethinyl-oestradiol and variable progesterone. The oestrogen content suppresses
the hypophyseal release of gonadotropins, which prevents the maturation of the
follicle, the ovulation and the luteinisation. The progesterone content favour
the secretion of sperm-hostile mucus in the uterus, inhibits tuba motility and
Side effects of the combined tablet are more
frequent in smoking female over 35 years, and in all females with
cardiovascular risk factors. Side-effects
are weight gain, accentuation of cervical and breast cancer, hypertension,
acute myocardial infarction, stroke, increased clotting capacity,
phlebothrombosis, gallstones, hepatomes, migraine, depression, impaired
glucose tolerance (Fig. 27-6), diabetes mellitus, hypercholesterolaemia, and
infertility. These serious side-effects are rare but still present.
Prescription of even the modern low risk pills necessitates careful control of
all risk factors.
Infertility is a diagnosis used on a couple, which have been
unable to conceive during one year of unprotected intercourse. The causes are
oligospermia, tuba blockage, ovulatory disorders, or combined problems with
both persons in the couple.
In some cases ovulation can be elicited by a
synthetic oestrogen receptor antagonist (clomiphene), which has a high affinity towards hypothalamic oestrogen
receptors. Clomifene administration simulates oestrogen deficiency in the
infertile patient with a hypothalamic defect, and by negative feedback
clomifene increases GnRH and FSH/LH secretion and promote fertility.
Impotence is frequently seen without organic cause such as hypogonadism. Diabetes
mellitus, essential hypertension, and neuropathy of the autonomic system cause
impotence just as antihypertensive drugs (diuretics, methylDOPA and b-blockers). Intracavernosal injections of prostaglandin E, papaverine,
phentolamine, and other vasodilatating substances can provide erection for a
few hours. The patient can use such a cocktail when needed.
disorders, such as benigh prostatic hypertrophy
and prostate cancer, increase in frequency with age above 60. Both disorders
interfere with micturition and can obstruct renal function leading to renal
insufficiency (Chapter 25). The enzyme 5a-reductase normally produces dihydrotestosterone from
testosterone. Inhibition of this enzyme minimises the hormone conversion and
causes the prostate to shrink.
cancer is frequently present in males with
elevated plasma concentrations of prostate-specific
antigen (PSA). Manifest prostate cancer is removed immediately. In a case
where surgery is containdicated, long acting GnRH agonists reduce testosterone
secretion and the growth of prostate cancer.
Menstrual disorders/Occlusion of the fallopian tube
Amenorrhoea or oligomenorrhoea are terms used for absence or irregularity of menstrual periods. Deficient
GnRH release prevent FSH secretion from recruiting a dominant follicle, and
complete loss of menses (amenorrhoea) may result. In oligomenorrhoea the
oestrogen secretion is sufficient for uterine bleeding to occur in an
irregular pattern, but often insufficient to induce a midcycle peak of LH and
Causes are ovarian disease or absence (Turners
syndrome, XO), hypothalamic deficiencies, congenital
adrenal hyperplasia (adrenogenital syndrome), and starvation amenorrhoea (anorexia nervosa and excessive exercise),
hypothyroid amenorrhoea with increased TRH and prolactin, and withdrawal
amenorrhoea (following oral contraception). Starvation amenorrhoea and anovulatory bleeding cycles often occur in
female long distance runners and ballet dancers, as well as in anorexia
nervosa patients (Chapter 7). These
females have lost substantial amounts of fat and suffer from a serious
oestrogen deficiency, which even may lead to osteoporosis (Chapter
of the fallopian tube
the start of the menstrual cycle the woman is given FSH to stimulate her
ovaries before ovulation. On the 12th day she is given hCG. When ovulation
occurs (after 30 to 35 hours), egg cells are sucked
out, placed in a tissue culture and exposed to spermatozoa. After 48
hours some eggs fertilise into the 4-8-cell stage. A few of these fertilised eggs are placed in the uterus. One in four of these eggs will nidate.
Therapy is directed towards the cause of the
The menopause is the event in the life of a female, where the menses stop. The last
ovulations are anovulatory and conception is no longer possible. The ovaries
become atrophic, the concentrations of pituitary gonadotropins (FSH more than
LH) in blood plasma and in urine are the highest in the life of the female,
because the follicles become more and more insensitive to gonadotropin
stimulation and the oestrogen and inhibin production diminishes. Functional
changes in other organs are less definitive, but vascular flushing of the head
and neck are typical, probably due to the release of large amounts of
hypothalamic gonadotropin releasing hormone (GnRH). Attacks of sweating during
the night are classical complains.
Adrenal and ovarian stromal cells secrete
androgen precursors that are converted to oestrogens by aromatase in adipose tissues. This is why menopausal females with
sufficient adipose tissue suffer less from oestradiol deprivation than lean
Females with severe complains are treated
with oestrogen, which ameliorates the disorders and reduces the rate of heart
disease and of postmenopausal
Osteoporosis or thin
bones is a term used for a
marked reduction in all elements of bone mass. Postmenopausal females reduce
their bone mass progressively with age up till the age of 70-75 years. This
bone reduction also occurs in elderly males, but at a much slower rate.
Elderly patients living indoors all year round are less exposed to sunshine
and do not synthesise vitamin D in the skin. If their diet simultaneously is
poor in vitamin D and Ca2+, it is not surprising that their bones
therapy is beneficial as a preventive strategy
in postmenopausal osteoporosis. So
is increased dietary Ca2+ with vitamin
D. Walking, jogging, golf are exercises retarding bone mass loss. Calcitonin has proven of benefit in some studies. A promising approach is the use of
oestrogen-receptor modulators to prevent osteoporosis and thrombo-embolic
events, without increasing the risk of breast cancer.
cancer tumours can be treated with synthetic blockers of the
oestrogen receptor. The blockers suppress the growth of oestrogen-sensitive
breast cancer. – Another therapy principle is to diminish oestrogen
production. This is done with the drug, aminoglutethimide, which inhibits the desmolase
reaction and thereby reduces adrenal steroid synthesis as a
blockers of the progesterone receptor (mifepristone) induces early
abortion by removing the positive progesterone effects on the conceptus.
following five statements have True/False options:
A. The menarche is the last menstrual bleeding.
have external genitals from both sexes, but only one gonadal sex.
means Human Immunodeficiency Virus. HIV is the cause of Acquired Immune
Deficiency Syndrome. HIV triggers a progressive and irreversible depletion of
love to dress like the opposite sex. Transvestites are heterosexual,
homosexual or asexual.
the onset of puberty a timing device in the brain triggers the Gonadotropin
producing machinery in the hypothalamic-pituitary axis.
24-year-old female is going through her last menstrual cycle before pregnancy.
1. Summarise schematically the most important hormonal events in her
schematically the most important hormonal events during continued pregnancy
pregnant woman delivers oxygen to her foetus. Her A‑haemoglobin (A =
adult) is functionally different from that of her foetus (F‑haemoglobin).
1. Why is this difference important? How are the two dissociation curves
2. FSH and LH are important for this woman. Describe why. Describe the
function of the two hormones in her husband.
3. Following birth the mother breastfeed her baby and experience a feeling
of sexual pleasure including uterine contractions. Describe the mechanism.
presence of normal ovaries or testes determines the gonadal sex. Without
normal ovaries or testes any genetic sex will develop into an apparent female.
brain is an important sex organ. The sex desire (libido) is stimulated by a
multitude of sense impressions (visual, auditive, olfactory, and
psychological). Potency refers to the ability to engage in intercourse.
· On the
first day of the menstrual bleeding, the low progesterone and high
prostaglandin level probably releases enough Ca2+ to start
spontaneous contractions of the myometrial cells. Ca2+ -ions enters
myometrial cells and stimulates their activity in the secretory (progesterone)
certain high plasma level of oestradiol can increase FSH output. This is
called the positive feedback release ovulation. At lower levels oestradiol is
a potent inhibitor of Gonadotropin-RH secretion and thus of FSH output
(negative feedback). The negative feedback forms the basis for the
ovulation-inhibition by contraceptives.
primary inhibitor of FSH secretion
is the peptide, inhibin that is secreted by the ovary and testis, and blocks
the effect of Gonadotropin-RH.
plasma [oestradiol] increases sharply in the last part of the follicular
phase, while the [LH] also increases. The sharp rise in LH and a modest rise
in FSH coincide with ovulation. The LH not only causes rupture of the
follicle; it continues to act on the follicular cells, turning them into a
yellow endocrine organ, the corpus luteum.
spermatozoa can keep their vitality for more than 4 days if they reach the
tube. They lose their protection cover in the uterine tube. The head of the
spermatozoa swell and liberates proteolytic enzymes. These enzymes dissolve
the corona radiata around the egg (oocyte). The oocyte can only live 14 hours
· Due to
the priming effect of oestrogen on progesterone receptors, both hormones
stimulate the growth of the endometrial glands, so that they curl like a
helix. The progesterone effect in particular provides the
endometrial/myometrial tissues with their high secretion and blood perfusion,
so the uterus is prepared to receive the fertilised ovum.
· The b-group
of hCG is specific and found in the blood by specific antibody methods even
before the first menstrual bleeding fails to appear. The hCG is detectable in
the urine 8-12 days after the first missing vaginal bleeding.
puberty FSH, LH, growth hormone, and insulin are important for the breast
development. The thyroid hormones (T3/T4) are
permissive. At the end of pregnancy there are other hormonal events.
Progesterone secretion reaches a peak and then falls. This fall in
progesterone allows the pituitary to release prolactin (LTH).
is a pro-insulin-like polypeptide produced by the corpus luteum. The hormone
relaxes pelvis articulations and softens the uterine cervix in order to
facilitate passage of the foetus. These and several other factors are involved
in human labour, but the exact trigger mechanism remains unclear.
described a syndrome in small apparent females, retarded in growth and in
sexual development, and with small or no ovaries. Since they have only one sex
chromosome (X), their total chromosome number is 45. They have no sex
chromatin and no drumstick.
described a syndrome in persons appearing as males. They are tall, have small
testes, some have female breasts (gynaecomastia), and they are sterile. Their cells contain XXY chromosomes (47 instead of the normal 46).
or oligomenorrhoea are terms used for absence or irregularity of menstrual
periods. Causes are ovarian
disease or absence (Turners syndrome, XO), hypothalamic deficiencies,
congenital adrenal hyperplasia (adrenogenital syndrome), starvation
amenorrhoea such as in anorexia nervosa and excessive exercise, hypothyroid
amenorrhoea with increased TRH, and withdrawal amenorrhoea (following oral
MH and BJ Everett. Essential
reproduction. 6th Ed. Blackwell Science, Oxford, 2007.
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