"Responding to follicle-stimulating hormone (FSH)
secretion from the pituitary gland, the granulose cells
of the ovarian follicles secrete gradually increasing levels
of estradiol, which peak around day 13, inducing the
pituitary LH surge that heralds ovulation. The intraovarian...
events leading to ovulation involve estrogen induced
production of prostaglandins, primarily
prostaglandin F2α (PGF2α), PGE2, and prostacyclin,
all of which are measurable in follicular fluid.
The release of this prostaglandin-rich fluid is thought to
cause the pain that sometimes occurs with ovulation....
With the decline of the corpus
luteum, estrogen and progesterone levels drop, triggering
the events in the uterine endometrium that lead to menstruation.
These events involve complex interplay of
prostaglandins, cytokines, and other lytic enzymes.
The endometrium also produces prostaglandins,
the predominant one being PGF2α, with lower levels
of PGE2 also produced. PGF2α release leads to
smooth muscle contraction, ischemia, and sensitization
of nerve endings; PGE2 is a smooth muscle relaxant.
Other molecules produced include endothelin-1,
metalloproteinases, TNF-α, and cytokines. Endometrial
prostaglandin levels are three times higher in the
luteal than in the follicular phase.
Levels are highest during menstruation, when most PGF2α release from
the endometrium occurs. Women who experience dysmenorrhea
have greater endometrial prostaglandin levels
than do asymptomatic women, and they have
higher levels of PGF2α in their menstrual fluid (35).
Prostaglandin production has been thought to influence
diarrhea associated with menses by inhibiting
transepithelial ion transport in the small intestine....
Altered prostaglandin levels can result in abdominal
pain, colonic contractions, and diarrhea....
Estrogen, TNF-α, endothelin, and prostaglandins also
exert effects on the GI tract. Estrogen receptors are
found throughout the GI tract (36) in components of
the pelvic floor (37) and in sensory neurons of the dorsal
root ganglia (38), suggesting that female sex hormones
may play a role in IBS symptomatology. Studies
have shown that estrogen and progesterone exert
many effects on the GI tract (36). These hormones
have a relaxing effect on the lower esophageal sphincter
and decrease colonic transit. TNF-α induces
inflammation, delays gastric emptying, increases
colonic transit time, and induces flow of fluid into GI
tissues. Endothelin has potent effects on GI smooth
muscle, leading to contraction of the esophagus, stomach,
and intestines, and has a modulatory effect on GI
motility (39). It also is a potent stimulator of gallbladder
motility, stimulates sphincter of Oddi motility, and
decreases trans-sphincteric flow (39)."
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