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Departments of 1 Obstetrics and Gynecology and 2 Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75235
Although it is
well known that progesterone alters uterine contractility and plays an
important role in maintenance of pregnancy, the biochemical mechanisms
by which progesterone alters uterine contractility in human gestation
are less clear. In this investigation we sought to identify
progesterone-induced adaptations in human myometrial smooth muscle
cells that may alter Ca2+
signaling in response to contractile agents. Cells were treated with
vehicle or the progesterone analog medroxyprogesterone acetate (MPA)
for 5 days, and intracellular free
Ca2+ concentration
([Ca2+]i)
was quantified after treatment with oxytocin (OX) or endothelin (ET)-1.
OX- and ET-1-induced increases in
[Ca2+]i
were significantly attenuated in cells pretreated with MPA in a
dose-dependent manner. Progesterone receptor antagonists prevented the
attenuated Ca2+ transients induced
by MPA. ETA and
ETB receptor subtypes were expressed in myometrial cells, and treatment with MPA resulted in
significant downregulation of ETA
and ETB receptor binding. MPA did
not alter ionomycin-stimulated increases in
[Ca2+]i
and had no effect on inositol trisphosphate-dependent or -independent release of Ca2+ from internal
Ca2+ stores. We conclude that
adaptations of Ca2+ homeostasis in
myometrial cells during pregnancy may include progesterone-induced
modification of receptor-mediated increases in
[Ca2+]i.
progesterone receptor; endothelin receptors; uterus; endothelin; oxytocin; antiprogestin; medroxyprogesterone acetate
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