PHYSIOLOGY AND

ENDOCRINOLOGY
OF
FEMALE
REPRODUCTION
•The reproductive process in a
women is a complex and highly
evolved interaction of many
components.

•The anatomic structures , the

hormonal components , and the
interaction between the two play
a vital role in the function of
reproductive system
 Index
1. Physiology –
Oogenesis
Menstrual cycle physiology
Sperm trans
Implantation.
2. Endocrinology- hormones related to
ovulation
pregnancy
parturition
 Hypothalamus
( releases GnRH)

Pituitary gland
( releases LH and FSH)

Ovary
( releases estrogen , progesterone; follicular
growth, ovulation , corpus luteum formation.

Uterus
(endometrial shedding or preparation for
pregnancy)
Oogenesis
Menstrual cycle Physiology
• In a normal menstrual cycle, orderly
cyclic hormone production and parallel
proliferation of uterine lining prepare
for implantation of embryo.
Menstrual cycle

Ovarian cycle Uterine cycle

Follicular Luteal Proliferative
secretory
 Normal Menses

• Most women (90%) have menstrual cycles with

an interval of 24 to 35 days
• Menarche is followed by approximately 5–7
years of increasing regularity as cycles shorten
to reach the usual reproductive age pattern.
• In the 40s, cycles begin to lengthen again.
• The usual duration of flow is 4–6 days, but
many women flow as little as 2 days and as
much as 8 days.
• The normal volume of menstrual blood loss is
30 mL; greater than 80 mL is abnormal
 Follicular phase
• Average length – 10-14 days
• Hormonal feedback promotes the orderly
development of a single dominant follicle ,
which should be mature at midcycle and
prepared for ovulation.
• The initial recruitment and growth of the
primordial follicle is gonadotropin
independent and affects a cohort over
several months.
• The stimuli responsible for the
recruitment and growth of the cohort of
follicles is unknown.
• At the primordial follicle stage, shortly after
initial recruitment, FSH assumes control of
follicular differentiation and growth and allows a
cohort of follicles to continue differentiation.
• This process signals the shift from gonadotropin-
independent to gonadotropin-dependent growth.
• The decline in luteal phase estrogen,
progesterone, and inhibin-A production by the
now-fading corpus luteum from the previous
cycle allows the increase in FSH that stimulates
this follicular growth .
• At this stage of development, identical cohort
members must either be selected for dominance
or undergo atresia. It is likely that the follicle
destined to ovulate was selected before this
point, although the mechanism for selection
remains obscure.
 Ovulation
• In the typical 28-day cycle, ovulation
occurs on cycle day 14.
• Rising estrogen levels have a negative
feedback effect on FSH secretion.
• The falling FSH level that occurs with the
progression of the follicular phase
represents a threat to continued follicular
growth.
• This process continues until all members
of the initial cohort, with the exception of
the single dominant follicle, have suffered
atresia. The stage is then set for ovulation
• At lower concentrations, estrogens inhibit LH
secretion. At higher levels, estrogen enhances
LH release.
• This stimulation requires a sustained high level
of estrogen (200 pg/mL) for more than 48
hours.
• Ovulation will occur in the single mature, or
Graafian, follicle 10 to 12 hours after the LH
peak or 34 to 36 hours after the initial rise in
midcycle LH.
• The midcycle LH surge is responsible for a
dramatic increase in local concentrations of
prostaglandins and proteolytic enzymes in the
follicular wall
• These substances progressively weaken the
follicular wall and ultimately allow a
 Luteal Phase
• Ovulation onset of menses
• Average length – 14days. This duration is
fixed.
• Variability in length of follicular phase is
responsible for most variations in total
cycle length.
• After ovulation, the remaining follicular
shell is transformed into the primary
regulator of the luteal phase: the corpus
luteum.
• the basement membrane of the corpus luteum
degenerates to allow proliferating blood
vessels to invade the granulosa-luteal cells in
response to secretion of angiogenic factors
such as vascular endothelial growth factor.
• This angiogenic response allows large amounts
of luteal hormones to enter the systemic
circulation.
• Corpus luteum steroids (estradiol and
progesterone) provide negative central
feedback and cause a decrease in FSH and LH
secretion.
• Continued secretion of both steroids will
decrease the stimuli for subsequent follicular
recruitment. Similarly, luteal secretion of
 In the absence of pregnancy

the corpus luteum regresses

estrogen and progesterone levels wane

central inhibition on gonadotropin

secretion removed

FSH and LH levels rise

recruit another cohort of follicles.

 If pregnancy occurs

placental hCG will mimic LH action

stimulate the corpus luteum to secrete

progesterone

this switch in the source of regulatory

progesterone production is referred
to as the luteal–placental shift.
LAYERS OF ENDOMETRIUM
 PROLIFERATIVE PHASE
• The proliferative phase is characterized by
progressive mitotic growth of the decidua
functionalis in preparation for implantation of
the embryo in response to rising circulating
levels of estrogen.
• At the beginning of the proliferative phase, the
endometrium is relatively thin (1--2 mm).
• The predominant change seen during this time
is evolution of the initially straight, narrow, and
short endometrial glands into longer, tortuous
structures.
• their organization changes from a low columnar
pattern in the early proliferative period to a
 SECRETORY PHASE
• Within 48 to 72 hours following ovulation, the
onset of progesterone secretion produces a
shift in histologic appearance of the
endometrium to the secretory phase, so named
for the clear presence of eosinophilic protein-
rich secretory products in the glandular lumen.
• During the secretory phase, the endometrial
glands form characteristic periodic acid–Schiff
positive–staining, glycogen-containing vacuoles
• These vacuoles initially appear subnuclearly
and then progress toward the glandular
lumen .
A. Early secretory phase- subnucleolar
vacuolation is prominent. Mitotic
activity is minimal.
B. Mid Secretory phase- the vacuoles
move to supranuclear portion and the
contents may be seen in the lumen.
• On approximately the seventh
postovulatory day, progressively the
stroma becomes looser and more
oedematous .
• Day 21 is regarded as the optimal time
for implantation.
• This change may be secondary to the
estrogen- and progesterone-mediated
increase in prostaglandin production by
the endometrium.
• An increase in capillary permeability is a
consequence of this local increase in
prostaglandins.
• Receptors for the sex steroids are
present in the muscular walls of the
endometrial blood vessels, and the
enzyme system for prostaglandin
synthesis is present in both the
muscular walls and the endothelium of
the endometrial arterioles.
• Mitoses are first seen in endothelial
cells on cycle day 22.
• The spiral arteries become clearly
visible and then progressively
lengthen and coil during the remainder
of the secretory phase.
• By around day 24, an eosinophilic-
staining pattern, known as cuffing, is
visible in the perivascular stroma.

• Eosinophilia then progresses to form

islands in the stroma followed by areas of
confluence.

• This staining pattern of the edematous

stroma is termed pseudodecidual
because of its similarity to the pattern
that occurs in pregnancy.
• Predecidual cells can be identified, initially
surrounding blood vessels, characterized
by cytonuclear enlargement, increased
mitotic activity, and the formation of a
basement membrane.
• The decidua, derived from stromal cells,
becomes an important structural and
biochemical tissue of pregnancy.
• Decidual cells control the invasive nature
of the trophoblast, and the products of the
decidua play important autocrine and
paracrine roles in fetal and maternal
tissues.
• Decidual cells aids in both the process of
endometrial bleeding (menstruation) and the
process of endometrial hemostasis
(implantation and placentation).
• Implantation requires endometrial hemostasis
and the maternal uterus requires resistance to
invasion. Inhibition of endometrial
hemorrhage canbe attributed, to a significant
degree, to appropriate changes in critical
factors as a consequence of decidualization.
• e.g., lower plasminogen activator levels,
reduced expression of the enzymes that
degrade the stromal extracellular matrix (such
as the metalloproteinases), and increased
levels of plasminogen activator inhibitor-1.
• C. Late Secretory phase- 2 days
before menses, there is a dramatic
increase in the number of
polymorphonuclear lymphocytes that
migrate from the vascular system.
• This leukocytic infiltration heralds the
collapse of the endometrial stroma
and the onset of the menstrual flow.
Early secretory Late secretory
endometrium endometrium
 MENSES
In the absence of implantation

glandular secretion ceases

destruction of the corpus luteum and

withdrawl of estrogen and progesterone

Irregular breakdown of the decidua

functionalis

The resultant shedding of this

Physiology of
endometrial
breakdown
1. The most prominent immediate effect of
this hormone withdrawal is a modest
shrinking of the tissue height and
remarkable spiral arteriole vasomotor
responses.
• blood flow within the spiral vessels
diminishes, venous drainage is
decreased, and vasodilatation ensues.
• Thereafter, the spiral arterioles undergo
rhythmic vasoconstriction and relaxation.
• Within the 24 hours immediately
preceding menstruation, these reactions
lead to endometrial ischemia and stasis.
2. Simultaneously, there is a breakdown of
lysosomes and a release of proteolytic
enzymes, which further promote local
tissue destruction.
• Their release is inhibited by
progesterone stabilization of the
lysosomal membranes. With the waning
of estrogen and progesterone levels, the
lysosomal membranes are not
maintained
• This layer of endometrium is then shed,
leaving the decidua basalis as the source
of subsequent endometrial growth.
3. Prostaglandins are produced throughout
the menstrual cycle and are at their
highest concentration during menses .
• Prostaglandin F2α (PGF2α) is a potent
vasoconstrictor, causing further arteriolar
vasospasm and endometrial ischemia.
• PGF2α produces myometrial contractions
that decrease local uterine wall blood
flow and may serve to expel physically the
sloughing endometrial tissue from the
uterus.
4. Progesterone withdrawal from
endometrial cells induces matrix
metalloproteinase secretion, which is
followed by the breakdown of cellular
membranes and the dissolution of
extracellular matrix.
• With the continuing progesterone
secretion of early pregnancy, the decidua
is maintained and metalloproteinase
expression is suppressed, in a mechanism
mediated by TGF-b.
• In a nonpregnant cycle, metalloproteinase
expression is suppressed after menses,
presumably by increasing estrogen levels
• TNF-a secretion by endometrial cells
reaches a peak at menstruation, but
there is no cycle change in receptor
content. TNF-a inhibits endometrial
proliferation and induces apoptosis.
• This cytokine causes a loss of adhesion
proteins (the cadherin-catenin-actin
complex) and induces cell-to-cell
dissolution.
• In addition to endometrial cells, TNF-a
alsocauses damage to vascular
endothelium.
 Mechanism of breakdown
ischemia and weakening progress

the continuous binding membrane is

fragmented

intercellular blood is extruded into the

endometrial cavity

• The process is initiated in the fundus

and extends throughout the uterus.
• Within 13 hours, the endometrial height
• Approximately 50% of the menstrual detritus is
expelled in the first 24 hours of menstrual flow.
• The menstrual fluid is composed of the
autolysed functionalis,inflammatory exudate,
red blood cells, and proteolytic enzymes (at
least one of which, plasmin, lyses fibrin clots as
they form)

• The basalis endometrium remains during

menses, and repair takes place from this layer.
• This endometrium is protected from the lytic
enzymes in the menstrual fluid by a mucinous
layer of carbohydrate products that are
discharged from the glandular and stromal
cells.
 A Teleologic Theory of Endometrial-Menstrual Events

• The teleologic view of menstrual

events was offered by Rock et al.
• The basic premise of this thesis is
that every endometrial cycle has, as
its only goal, nourishing support of an
early embryo.
• Failure to accomplish this objective is
followed by orderly elimination of
unutilized tissue and prompt renewal
to achieve a more successful cycle
Sperm Transport
• 1. Approximately 72 days are
required to produce spermatozoa, a
time period followed by storage in
the epididymis prior to ejaculation.
• 2. Sperm enter the cervical mucus
and then the fallopian tubes within
minutes, but only a few hundred
sperm or less reach the oocyte. The
cervix serves as a reservoir of sperm
for up to 72 hours.
• 3. Capacitation, a process initiated during
the sperm's passage through the cervix or
during in vitro incubation in an appropriate
medium, is characterized by the acquired
ability of sperm to undergo the acrosome
reaction to bind to the zona pellucida and
to acquire hyperactivated motility.
• 4. The acrosome reaction is due to the
modification and breakdown, followed by a
merger, of the sperm cell membrane and
the outer acrosomal membrane, allowing
the release of enzymes and changes in the
inner acrosomal membrane, necessary for
fusion with the oocyte cell membrane
 Egg Transport
1. After ovulation, the oocyte and its
surrounding cumulus are in the ampulla of
the fallopian tube within 2–3 minutes.
2. Tubal transport depends on smooth
muscle contractions and ciliary-induced
flow of secretory fluid.
3. The fallopian tube provides an important
holding action to allow time for the
endometrium to become receptive and the
blastocyst to become capable of
implantation, a time period of
approximately 80 hours, 90% of which is in
the ampulla.
Fertilization
1.Sperm penetration of the zona pellucida
depends on a combination of sperm
motility, an acrosomal proteinase, and
binding of sperm head receptors to zona
ligands.

2. Binding of sperm head receptors and

zona ligands produces an enzyme complex
that induces the acrosome reaction,
releasing enzymes essential for the fusion
of the sperm and oocyte membranes.
3.Fusion of the sperm and oocyte
membranes triggers the cortical reaction,
the release of substances from the cortical
granules, organelles just below the egg
cell membrane.
4. The cortical reaction leads to the
enzyme-induced zona reaction, the
hardening of the zona and the inactivation
of ligands for sperm receptors, producing
an obstacle to polyspermy.
5. Cell division begins promptly after
fertilization; human gene expression
begins between the 4- and 8-cell stages.
 Implantation
1. The early embryo enters the uterine cavity
as an 8-cell morula and becomes a 30 to 200-
cell blastocyst before implantation.
2. Implantation begins with hatching from the
zona pellucida about 1–3 days after the
morula entered the uterine cavity.
3. The endometrium is prepared for
implantation by the complex activity of
cytokines, growth factors, and lipids
modulated by the sex hormones, especially
progesterone. The endometrium is receptive
for implantation for only a few days.
4. The process of implantation begins with apposition and
adhesion of the blastocyst to the uterine epithelium, about
2–4 days after the morula enters the uterine cavity.

• This process is mediated by cytokines and involves

adhesion molecules (integrins) that interact with
extracellular components, especially laminin and
fibronectin.

5. Trophoblastic invasion rapidly follows adhesion of the

blastocyst, mediated by proteinase degradation of the
extracellular matrix.
• The placenta is formed in the second week after ovulation.
• Limitation of trophoblastic invasion is due to a restraint
imposed by proteinase inhibitors, especially plasminogen
activator inhibitor and tissue inhibitors of
metalloproteinases.
 Hormones
related to
female
reproduction
 Gonadotrophin Releasing Hormone

• GnRH (also called luteinizing hormone–

releasing hormone, or LHRH) is the
controlling factor for gonadotropin secretion .
• It is a decapeptide produced by neurons with
cell bodies primarily in the arcuate nucleus of
the hypothalamus .
• It is unique among the body’s hormones
because it must be secreted in a pulsatile
fashion to be effective, and the pulsatile
release of GnRH influences the release of the
twogonadotropins
• The continual pulsatile secretion of GnRH
is necessary because GnRH has an
extremely short half-life (only 2–4 minutes)
as a result of rapid proteolytic cleavage.
• Continual exposure of the pituitary
gonadotroph to GnRH results in a
phenomenon called down-regulation,
through which the number of gonadotroph
cell surface GnRH receptors is decreased.
• intermittent exposure to GnRH will “up-
regulate” or “autoprime” the gonadotroph
to increase its number of GnRH receptors .
• This allows the cell to have a greater
response to subsequent GnRH exposure.
• The follicular phase is characterized by frequent,
small-amplitude pulses of GnRH secretion.
• In the late follicular phase, there is an increase in
both frequency and amplitude of pulses.
• During the luteal phase, however, there is a
progressive lengthening of the interval between
pulses.
• The amplitude in the luteal phase is higher than
that in the follicular phase, but it declines
progressively over the 2 weeks. This variation in
pulse frequency allows for variation in both LH
and FSH throughout the menstrual cycle.
• For example, decreasing the pulse frequency of
GnRH decreases LH secretion but increases FSH,
an important aspect of enhancing FSH availability
in the late luteal phase.
 Gonadotrophins
• The gonadotropins FSH and LH are
produced by the anterior pituitary
gonadotroph cells which are
responsive to the pulsatile
stimulation by GnRH.
• They are responsible for ovarian
follicular stimulation.
• GnRH and gonadotropin secretion are always
pulsatile in nature, but an augmentation of
the pulsatile pattern of gonadotropin
secretion occurs just before puberty with
nighttime increases in LH.
• After puberty, enhanced pulsatile secretion
is maintained throughout the 24-hour period,
but it varies in both amplitude and frequency.
• In puberty, arcuate activity begins with a low
frequency of GnRH release and proceeds
through a cycle of acceleration of frequency,
characterized by passage from relative
inactivity, to nocturnal activation, to the full
adult pattern.
• Structurally, there is great similarity
between FSH and LH .
• They are both glycoproteins that share
identical α subunits and differ only in the
structure of their β subunits, which
confer receptor specificity .
• The synthesis of the β subunits is the
rate-regulating step in gonadotropin
biosynthesis .
• Thyroid-stimulating hormone and
placental hCG also share identical α
subunits with the gonadotropins.
• The gene for the a subunit of the
gonadotropins is expressed in both the
pituitary and placenta.
• The b-subunit for human chorionic
gonadotropin (HCG) is expressed in the
placenta but only minimally (and with
alterations in structure) in the pituitary
• The LH b-subunit is expressed in the
pituitary but not significantly in the
placenta.
• Binding of GnRH to its receptor in the
pituitary activates multiple messengers and
responses.
• The immediate event is a secretory release
of gonadotropins, while delayed responses
prepare for the next secretory release.
• One of these delayed responses is the self-
priming action of GnRH that leads to even
greater responses to subsequent GnRH
pulses.
• This self-priming action is important to
achieve the large surge in secretion at
midcycle; it requires estrogen exposure, and
it can be augmented by progesterone.
• Low levels of estrogen enhance FSH and LH
synthesis and storage, have little effect on LH
secretion, and inhibit FSH secretion.
• High levels of estrogen induce the LH surge at
midcycle, and high steady levels of estrogen lead
to sustained elevated LH secretion.
• Low levels of progesterone acting at the level of
the pituitary gland enhance the LH response to
GnRH and are responsible for the FSH surge at
midcycle.
• High levels of progesterone inhibit pituitary
secretion of gonadotropins by inhibiting GnRH
pulses at the level of the hypothalamus.
• In addition, high levels of progesterone
antagonize pituitary response to GnRH by
interfering with estrogen action.
Gonadotrophin secretion
 Prolactin
• Prolactin, a 198–amino acid polypeptide
secreted by the anterior pituitary lactotroph,
is the primary trophic factor responsible for
the synthesis of milk by the breast.
• Prolactin secretion is under tonic inhibitory
control by the hypothalamic secretion of
dopamine.
• Prolactin appears to be primarily under
inhibitory control, many stimuli can elicit its
release, including breast manipulation, drugs,
stress, exercise, and certain foods.
• Prolactin gene expression occurs in the
lactotrophs of the anterior pituitary
gland, in decidualized endometrium, and
the myometrium.
• The secretion of prolactin is inhibited and
stimulated by the association and
dissociation of dopamine from its
receptors.
• Several factors exert a stimulatory effect
on prolactin secretion (prolactin-releasing
factors), especially TRH, vasoactive
intestinal peptide (VIP), epidermal growth
factor, and perhaps GnRH.
Function :
• lactogenesis in breast alveolar
epithelium
• After parturition – prolsctin induces milk
secretion – inhibitory influence of high
estrogen and progesterone withdrawn.
 Secretion :
• Very low in childhood , increases in girls
at puberty
• High in adult females, progressively
increase in pregnancy and peak at term.
 Oxytocin
• Oxytocin is a 9–amino acid peptide
primarily produced by the paraventricular
nucleus of the hypothalamus .
• The primary function of this hormone in
humans is the stimulation of two specific
types of muscular contractions.
• The first type, uterine muscular
contraction, occurs during parturition.
• The second type of muscular contraction
regulated by oxytocin is breast lactiferous
duct myoepithelial contractions, which
occur during the milk letdown reflex.
• Oxytocin release may be stimulated
by –
suckling, triggered by a signal from
nipple stimulation transmitted via
thoracic nerves to the spinal cord
and then to the hypothalamus,
where oxytocin is released in an
episodic fashion.
• Stimulation of the cervix and vagina
can cause significant release of
oxytocin,which may trigger further
oxytocin release from pituitary(the
Ferguson reflex).
 Estrogen
• Estrogen, or oestrogen, is the
primary Female sex hormone.
• There are three major endogenous estrogens
in females that have estrogenic hormonal
activity: estrone, estradiol, and estriol. The
estrane steroid estradiol is the most potent
and prevalent of these.
• Another type of estrogen called estetrol (E4)
is produced only during pregnancy.
Biosynthesis -
• Estrogens, in females, are produced primarily by
the ovaries, and during pregnancy, the placenta.
• Glandular estrogen synthesis: occurs in the granulosa and
theca cells of the ovaries, as well as the corpus luteum
– The granulosa cells are stimulated by LH to produce
pregnenolone
• Pregnenolone diffuses out of these cells to adjacent theca cells
• Theca cells express 17,20-lyase and 3β-HSD, which mediate the
conversion of pregnenolone to androstenedione via DHEA
• Most androstenedione returns to the granulosa cells and is converted to
estrone by aromatase, which is then converted to estradiol by 17β-HSD
– The expression of aromatase and 17β-HSD is controlled by FSH
stimulation
• Extraglandular synthesis: Aromatase is expressed in non-
gonadal sites and facilitates peripheral aromatization of
androgens to estrone.
– Fat cells: increases serum estrogens by converting androgen to
estrone.
– Bone: converts testosterone to local estrogen to help mature the
epiphyses.
Two cell – two gonadotrophin
theory
• Two classes of ER exist: nuclear estrogen
receptors (ERα and ERβ), which are members of
the nuclear receptor family
of intracellular receptors.
• The ERα is found
in endometrium ,breast ,cancer cells, ovarian
stromal cells, and the hypothalamus. In
males, ERα protein is found in the epithelium of
the efferent ducts.
• The expression of the ERβ protein has been
documented in ovarian granulosa cells , kidney ,
brain , bone, heart , lungs , intestinal
mucosa, prostate, and endothelial cells.
 Progesterone
• Progesterone is an endogenous
steroid and progestogen sex hormone involved in
the menstrual cycle , pregnancy and
embryogenesis of humans and other species.
• Progesterone has a number of physiological
effects that are amplified in the presence
of estrogens. Estrogens through estrogen
receptors (ERs) induce
or upregulate the expression of the PR.
• One example of this is in breast tissue, where
estrogens allow progesterone to
mediate lobuloalveolar development.
Progestin synthesis
• Progesterone is synthesized from pregnenolone by
action of 3β-HSD in the corpus luteum, by the placenta
during pregnancy; as well as by the adrenals, as a step
in androgen and mineralocorticoid synthesis.
• Its actions are primarily mediated by an intracellular
progesterone receptor, whose numbers increase in the
presence of estrogen.
• The products of hormone synthesis vary with the
menstrual cycle; estradiol is the main product during
follicular maturation, whereas progesterone is the main
product in the luteal phase following ovulation.
 Functions of progesterone
• Progesterone plays several important actions in the normal
female reproductive cycle:
– Prepares the uterus for pregnancy by shifting the endometrium
from proliferation to secretion.
– Withdrawal of progesterone in the absence of pregnancy leads to
organized shedding (menstruation).
– Helps mediate sexual response in the brain.
• After fertilization, progesterone:
– Organizes the vasculature of the endometrium to prepare for
implantation
– Promotes enzymatic digestion of the zona pellucida to allow the
oocyte to implant into the uterine wall
– Inhibits contractions of the uterine myometrium (smooth muscle
layer) and counteracts the effects of oxytocin on contractility
– Promotes lobuloalveolar growth in the breasts to prepare for
lactation, but suppresses premature milk protein synthesis prior
to parturition
• Some of the effects of progesterone may be
related to its ability to antagonize estrogen
by decreasing expression of estrogen
receptors, e.g. the ability of progesterone to
inhibit estrogen-mediated endometrial
proliferation
• Progesterone also has a potent effect as an
antagonist of the mineralocorticoid receptor,
reducing sodium retention when present,
and increasing sodium retention when
progesterone is withdrawn.
Endocrinology of Pregnancy
 Estrogen
• Estrogen influences progesterone
production, uteroplacental blood flow,
mammary gland development, and fetal
adrenal gland function.
• The fetal adrenal provides DHAS as
precursor for placental production of estrone
and estradiol.
• The fetal adrenal, with the aid of 16a-
hydroxylation in the fetal liver, provides the
16a-hydroxydehydroepiandrosterone sulfate
for placental estriol formation.
• Estriol is the estrogen produced in
greatest quantity during pregnancy;
estrone and estradiol are derived
equally from fetal and maternal
precursors.
• It is found in the urine of pregnant
women and placenta.
 Progesterone
• Progesterone is largely produced by the
corpus luteum until about 10 weeks of
gestation. Indeed, until approximately the
7th week, the pregnancy is dependent upon
• the presence of the corpus luteum.1
Exogenous support for an early pregnancy
(until 10 weeks) requires 100 mg of
progesterone daily, associated with a
maternal circulating level of approximately
10 ng/mL.
• After a transition period of shared
function between the 7th week and 10th
week during which there is a slight
decline in circulating maternal
progesterone levels, the placenta
emerges as the major source of
progesterone synthesis and maternal
circulating levels progressively
increase.
• The majority of placental progesterone
is derived from maternal cholesterol
that is readily available.
• It has been suggested that progesterone is
important in suppressing the maternal
immunological response to fetal antigens,
thereby preventing maternal rejection of the
trophoblast.
• Progesterone prepares and maintains the
endometrium to allow implantation.
• Because implantation normally occurs about 5–
6 days after ovulation, and human chorionic
gonadotropin (HCG) must appear by the 10th
day after ovulation to rescue the corpus luteum,
the blastocyst must successfully implant and
secrete HCG within a narrow window of time.
• In the first 5–6 weeks of pregnancy, HCG
stimulation of the corpus luteum results in the
daily secretion of about 25 mg of progesterone
and 0.5 mg of estradiol.
 RELAXIN

• In females relaxin is produced mainly by the corpus luteum, in

both pregnant and nonpregnant females; it rises to a peak
within approximately 14 days of ovulation, and then declines
in the absence of pregnancy, resulting in menstruation.
• During the first trimester of pregnancy, levels rise and
additional relaxin is produced by the decidua.
• Relaxin's peak is reached during the 14 weeks of the first
trimester and at delivery.
• It is known to mediate the hemodynamic changes that occur
during pregnancy, such as increased cardiac output,
increased renal blood flow, and increased arterial compliance.
• It also relaxes other pelvic ligaments.
• It is believed to soften the pubic symphysis.
 Human chorionic gonadotropin
hormone
• HCG gene expression is present in both
cytotrophoblast and syncytiotrophoblast, but it is
synthesized mainly in the syncytiotrophoblast
• Continued survival of the corpus luteum is totally
dependent on HCG, and, in turn, survival of the
pregnancy is dependent upon steroids from the
corpus luteum until the 7th week of pregnancy.
• From the 7th week to the 10th week, the corpus
luteum is gradually replaced by the placenta, and
by the 10th week, removal of the corpus luteum
will not be followed by steroid withdrawal
abortion.
• HCG concentration is approximately
100 IU/L at the time of the expected
but missed menses. A maximal level
of about 100,000 IU/L in the
maternal circulation is reached at 8–
10 weeks of gestation.
• HCG levels decrease to about
10,000–20,000 IU/L by 18–20 weeks
and remain at that level to term.
Functions-
• Human chorionic gonadotropin interacts with the HCG
receptor of the ovary and promotes the maintenance of
the corpus luteum during the beginning of pregnancy.
• Due to its highly negative charge, hCG may repel the
immune cells of the mother, protecting the fetus during
the first trimester
• It has also been suggested that hCG levels are linked to
the severity of morning sickness or hyperemesis
gravidarum in pregnant women.[
• Human chorionic gonadotropin hormone(hCG) enhances
maternal breast growth by increasing protein synthesis.
• HCG increases maternal fatty acid for ATP production,
leaving more glucose available for Fetus.
 Human Placental Lactogen

• Human placental lactogen, also known as human

chorionic somatomammotropin, is produced and
secreted by the syncytiotrophoblast of the placenta.
It is structurally and functionally related to GH.
• A major role is the GH-like effect in inducing
resistance to insulin action in the mother. This limits
maternal glucose utilization, while ensuring an
appropriate supply of free fatty acids derived from
lipolysis for the mother during fasting, sparing
glucose for fetal energy needs to protect against fetal
hypoglycemia.
• A possible role for human placental lactogen to
promote fetal growth by stimulating amino acid
uptake, DNA synthesis, and IGF-I production has also
been suggested.
 Corticotropin hormone-releasing
hormone
• Corticotropin-releasing hormone (CRH) also known as
corticotropin-releasing factor (CRF) or corticoliberin is a
peptide hormone and neuro transmitter involved in the
stress response.
• It belongs to corticotropin- releasing factor family.
• In humans, it is encoded by the CRH gene.
• CRH is secreted by the para ventricular nucleus (PVN) of
the hypothalamus in response to stress.
• FUNCTION OF CORTICOTROPIN HORMONE-RELEASING
HORMONE
 CRH is also synthesized by the placenta and seems to
determine the duration of pregnancy.
 In the placenta, CRH is a marker that determines the length
of gestation and the timing of parturition and delivery.
 CRH may act as a trigger for parturition
 OXYTOCIN HORMONE

• The hormone oxytocin plays a key role in labour.

Often called the ‘love hormone’, oxytocin is
associated with feelings of bonding and motherhood.
• This is also true of another hormone released during
labour called prolactin.
• If labour needs to be induced oxytocin or a synthetic
oxytocin equivalent is often administered to ‘kick-
start’ the process.
• Oxytocin levels rise at the onset of labour, causing
regular contractions of the uterine and abdominal
muscles.
• Oxytocin induced contractions become stronger and
more frequent without the influence of progesterone
and oestrogen, which at high levels prevent labour.
 CONCLUSION
• . It is concluded that, the whole process of
ovulation, pregnancy and parturation, occurs
under the influence of hormones.
• Hormonal regulation play important role in all
these processes.
• Imbalance of any one hormone out of all these
hormones, can affect the all these processes.
• Hormones are regulated by pitutary gland of
hypothalamus.
• Releasing time of also important so that at
particular time the hormone level is same as it
required for complete process.