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Abstract
Ovariectomized early pregnant rats given continuous steroid replacement therapy have
been treated with antiprogesterone steroid, ZK98299 or RU38486. At 24 h following
treatment, uterine explants in culture were found to produce significantly greater
amounts of PGF2α, but not of 6-keto-PGF1α, when compared to controls. ZK98299 and RU38486 gave almost identical levels of uterine
PG production. The ![Math Eq]()
production ratio for uteri of treated rats was decreased by 45% relative to controls.
Similar changes in uterine PGF2α production and ![Math Eq]()
ratio have been shown for ovariectomized early pregnant rats in which progesterone
has been withdrawn when compared to control animals. It has been suggested that inhibiting
or withdrawing progesterone in rat uteri exposed to estradiol and progesterone may
lead to a stimulation of endoperoxide F-reductase and/or E2 9-ketoreductase activities. The presence of luminal fluid in the uteri was observed
for animals treated with antiprogesterone steroid or in which progesterone had been
withdrawn. This was associated with a decrease in % dry weight for the uteri of these
animals.
production ratio for uteri of treated rats was decreased by 45% relative to controls.
Similar changes in uterine PGF2α production and 
ratio have been shown for ovariectomized early pregnant rats in which progesterone
has been withdrawn when compared to control animals. It has been suggested that inhibiting
or withdrawing progesterone in rat uteri exposed to estradiol and progesterone may
lead to a stimulation of endoperoxide F-reductase and/or E2 9-ketoreductase activities. The presence of luminal fluid in the uteri was observed
for animals treated with antiprogesterone steroid or in which progesterone had been
withdrawn. This was associated with a decrease in % dry weight for the uteri of these
animals.To read this article in full you will need to make a payment
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Article info
Publication history
Accepted:
July 4,
1991
Received:
April 26,
1991
Identification
Copyright
© 1991 Published by Elsevier Inc.
