Chapter 27
The Reproductive System
end of the cycle (days 26–28) ends their blockade of FSH and
LH secretion, and the cycle starts anew.
We have just described ovarian events as if we are following
one follicle through the 28-day cycle, but this is not really the
case. What is happening is that the increase of FSH at the begin-
ning of each cycle allows several vesicular follicles to continue to
mature. Ten, with the midcycle LH surge, one (or more) vesic-
ular follicles undergo ovulation. However, the ovulated oocyte
would actually have been activated up to 12 months before, not
14 days before.
The Uterine (Menstrual) Cycle
Although the uterus is where an embryo implants and devel-
ops, it is receptive to implantation for only a short period each
month. Not surprisingly, this brief interval is exactly the time
when a developing embryo would normally begin implanting,
six to seven days a±er ovulation. Te
, or
is a series of cyclic changes that the uter-
ine endometrium goes through each month as it responds to the
waxing and waning of ovarian hormones in the blood. Tese
endometrial changes are coordinated with the phases of the
ovarian cycle, which are dictated by gonadotropins released by
the anterior pituitary.
Changes in ovarian steroid hormone levels drive the events
of the uterine cycle
(Figure 27.22d)
as follows:
Days 1–5: Menstrual phase.
In this phase,
shun) or
, the uterus sheds all but the
deepest part of its endometrium. (Note in Figure 27.22a
and c that at the beginning of this stage, ovarian hormones
are at their lowest normal levels and gonadotropins are
beginning to rise.) Te thick, hormone-dependent func-
tional layer of the endometrium detaches from the uterine
wall, a process accompanied by bleeding for 3–5 days. Te
detached tissue and blood pass out through the vagina as
the menstrual flow. By day 5, the growing ovarian follicles
start to produce more estrogen (Figure 27.22c).
Days 6–14: Proliferative (preovulatory) phase.
In this
phase, the endometrium rebuilds itself: Under the influ-
ence of rising blood levels of estrogens, the basal layer of
the endometrium generates a new functional layer. As
this new layer thickens, its glands enlarge and its spiral
arteries increase in number (also see Figure 27.15). Con-
sequently, the endometrium once again becomes velvety,
thick, and well vascularized. During this phase, estro-
gens also induce the endometrial cells to synthesize pro-
gesterone receptors, readying them for interaction with
Normally, cervical mucus is thick and sticky, but ris-
ing estrogen levels cause it to thin and form channels that
facilitate sperm passage into the uterus.
, which
takes less than five minutes, occurs in the ovary at the end
of the proliferative stage (day 14) in response to the sud-
den release of LH from the anterior pituitary. As we saw
earlier, LH also converts the ruptured follicle to a corpus
follicle maturation.
, released by the granulosa cells,
also exerts negative feedback controls on FSH release dur-
ing this period. Only the dominant follicle survives this dip
in FSH—the other developing follicles fail to develop fur-
ther, and they deteriorate.
Positive feedback stimulates gonadotropin release.
though the initial small rise in bloodborne estrogen inhibits
the hypothalamic-pituitary-gonadal axis, the high estrogen
level produced by the dominant follicle has the opposite ef-
fect. Once estrogen reaches a critical blood concentration,
it briefly exerts
positive feedback
on the brain and anterior
LH surge triggers ovulation and formation of the corpus
Te high estrogen level sets a cascade of events into
motion. Tere is a sudden burstlike release of accumulated
LH (and, to a lesser extent, FSH) by the anterior pituitary
about midcycle (also see Figure 27.22a).
Te LH surge rouses the primary oocyte of the domi-
nant follicle from its resting state and it completes its first
meiotic division, forming a secondary oocyte that contin-
ues on to metaphase II. Around day 14, LH—aided by in-
traovarian paracrine factors—stimulates many events that
lead to ovulation: It increases local vascular permeability
and triggers an inflammatory response that promotes re-
lease of metalloproteinase enzymes that weaken the ovary
wall. As a result, blood stops flowing through the protrud-
ing part of the follicle wall. Within minutes, that region of
the follicle wall thins, bulges, and ruptures, forming a hole
Te oocyte, still surrounded by its corona ra-
diata, exits, accomplishing ovulation. Te role (if any) of
FSH in this process is unknown.
Shortly a±er ovulation, estrogen levels decline. Tis
probably reflects the damage to the dominant estrogen-
secreting follicle during ovulation.
Te LH surge also transforms the ruptured follicle into a
corpus luteum (which gives LH its name, “luteinizing” hor-
mone). LH stimulates this newly formed endocrine struc-
ture to produce large amounts of progesterone and some
estrogen almost immediately a±er it is formed. Progester-
one helps maintain the stratum functionalis and is essential
for maintaining pregnancy should conception occur.
Negative feedback inhibits LH and FSH release.
Rising pro-
gesterone and estrogen blood levels exert a powerful nega-
tive feedback effect on the hypothalamus and the anterior
pituitary release of LH and FSH. Inhibin, released by the
corpus luteum and granulosa cells, enhances this inhibitory
effect. Declining gonadotropin levels inhibit the matura-
tion of new vesicular follicles and prevent additional LH
surges that might cause additional oocytes to be ovulated.
In cycles in which fertilization does not occur, the stimulus
for luteal activity ends when LH blood levels fall and the corpus
luteum degenerates. As goes the corpus luteum, so go the levels
of ovarian hormones, and blood estrogen and progesterone lev-
els drop sharply. Te marked decline in ovarian hormones at the
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