Fluprostenol-induced softening of the cervix of the pregnant rat

1983 ◽  
Vol 97 (2) ◽  
pp. 283-290 ◽  
Author(s):  
L. M. Williams ◽  
M. Hollingsworth ◽  
M. Dukes ◽  
I. D. Morris
Keyword(s):  
Binding Capacity ◽  
Direct Action ◽  
Prostaglandin E ◽  
Uterine Contractility ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Uterine Contractions ◽  
Prostaglandin F

Fluprostenol, an analogue of prostaglandin F2α, administered s.c. to rats on day 18 of pregnancy increased cervical creep, or softness, by the following day. Doses of fluprostenol 100-fold larger were necessary to increase uterine contractions. Fluprostenol produced falls in serum progesterone concentrations, increases in 20α-dihydroprogesterone concentrations, no changes in oestradiol or relaxin concentrations and a reduction in the ovarian human chorionic gonadotrophin binding capacity in vitro. Fluprostenol was less potent in inducing cervical softness when administered per vaginam, and a dose which produced softening in pregnant rats was ineffective in ovariectomized steroid-maintained pregnant or pro-oestrous rats. The findings suggest that cervical softening by fluprostenol does not result from a simple direct action on the cervix or by increasing uterine contractions, but rather by an indirect hormonal action mediated by the ovaries. The results with the lowest dose of fluprostenol indicate that cervical softening could be produced without a sustained fall in serum progesterone concentrations. Fluprostenol is much more potent at increasing cervical softness in the pregnant rat than prostaglandin F2α or prostaglandin E2. With fluprostenol the ratio of dose to induce uterine contractility relative to that to produce cervical softness was greater than with these natural prostaglandins, indicating the greater selectivity of fluprostenol in the pregnant rat.

Inhibition by prostaglandin E2of the release of vasopressin and β-endorphin from rat pituitary neurointermediate lobe or medial basal hypothalamus in vitro

1985 ◽  
Vol 106 (2) ◽  
pp. 189-195 ◽  
Author(s):  
W. Knepel ◽  
D. Nutto ◽  
M. Vlaskovska ◽  
Ch. Kittel
Keyword(s):  
Direct Action ◽  
Effective Concentration ◽  
Neurosecretory System ◽  
Intermediate Lobe ◽  
Medial Basal Hypothalamus ◽  
Neurointermediate Lobe ◽  
Rat Pituitary ◽  
Prostaglandin F ◽  
Spontaneous Secretion

ABSTRACT The present study was performed to examine the effect of the cyclo-oxygenase inhibitor, indomethacin, and that of various prostaglandins on the release of vasopressin and β-endorphin-like immunoreactivity (β-EI) from the rat neurointermediate lobe of the hypophysis, which was superfused in vitro. Indomethacin (2·8 and 28 μmol/l) changed neither basal secretion of vasopressin nor that evoked by electrical stimulation, whereas the resting release of β-EI was enhanced by indomethacin (28 μmol/l). Prostaglandin (PG) E2 did not influence resting release of vasopressin but markedly inhibited (by about 50%) electrically induced release of vasopressin (least effective concentration: 300 nmol/l) as well as spontaneous secretion of β-EI (least effective concentration: 100 nmol/l) in the presence of indomethacin (28 μmol/l). Prostaglandin F2α (5 μmol/l) also inhibited the evoked release of vasopressin, whereas PGD2 (5 μmol/l) did not. Prostaglandin F2α (5 μmol/l), D2 and I2 (1·5 μmol/l each) produced no effects on β-EI release. As observed in the neurohypophysis, PGE2 inhibited the electrically induced release of vasopressin from the medial basal hypothalamus in vitro. We conclude that prostaglandins (especially PGE2) can inhibit (1) the stimulated release of vasopressin when acting on vasopressin-containing nerve terminals of either neurosecretory system (neurohypophysis, median eminence region), and (2) the secretion of β-EI and, as can be inferred, α-MSH, by a direct action on intermediate lobe cells. J. Endocr. (1985) 106, 189–195

Role of interleukin-1β in the regulation of porcine corpora lutea during the late luteal phase of the cycle and during pregnancy

2012 ◽  
Vol 60 (3) ◽  
pp. 395-407 ◽  
Author(s):  
Agata Zmijewska ◽  
Anita Franczak ◽  
Genowefa Kotwica
Keyword(s):  
Secretory Activity ◽  
Oestrous Cycle ◽  
Interleukin 1Β ◽  
Prostaglandin E ◽  
Corpora Lutea ◽  
Prostaglandin Synthase ◽  
Late Luteal Phase ◽  
Prostaglandin F ◽  
Hormonal Milieu

Interleukin-1β (IL-1β) may regulate ovarian physiology. In this study, the influence of IL-1β on secretory activity within the corpora lutea (CL) of cyclic and gravid pigs was determinedin vitroduring different stages of the CL lifespan, e.g. on Days 10–11, 12–13 and 15–16 of the oestrous cycle and pregnancy. IL-1β (10 ng/ml) increased prostaglandin E2(PGE2) secretion from CL of the cyclic and gravid pigs during studied days of the oestrous cycle and pregnancy. Increase (P < 0.05) of prostaglandin F2α(PGF2α) in IL-1β-treated CL was demonstrated only on Days 10–11 of the oestrous cycle. More potent stimulatory effect of IL-1β on PGE2than PGF2αsecretion resulted in the enhancement of the PGE2:PGF2αratio in cyclic and early pregnant CL. IL-1β increased (P < 0.05) progesterone (P4) secretion only in gravid CL and had no effect on oestradiol-17β (E2) release. Expression of cyclooxygenase-2 (COX-2) mRNA was stimulated (P < 0.05) in IL-1β-treated cyclic and gravid CL. Expression of prostaglandin synthase mRNAs in response to IL-1β did not increase. In conclusion, IL-1β modulates PGE2, PGF2αand P4secretion from porcine CL, depending on luteal stage and the surrounding hormonal milieu. The cytokine may act locally in porcine CL for luteotrophic support throughout the PGE2-mediated synthesis and secretion.

scholarly journals Hormonal control of Luteal 20α-Hydroxy steroid dehydrogenase and Δ5-3β-hydroxy steroid dehydrogenase during luteolysis in the pregnant rat

1975 ◽  
Vol 152 (3) ◽  
pp. 433-443 ◽  
Author(s):  
R G Rodway ◽  
N J Kuhn
Keyword(s):  
Prostaglandin F2α ◽  
Late Pregnancy ◽  
Normal Pregnancy ◽  
Hormonal Control ◽  
Placental Lactogen ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Hydroxy Steroid ◽  
Steroid Dehydrogenase

Treatment of pregnant rats with human chorionic gonadotrophin, luteotrophin (luteinizing hormone), luteotrophin-releasing hormone, prostaglandin F2α, aminoglutethimide, or by foetoplacental removal or hysterectomy achieved a common multiple-response pattern, namely increased activity of luteal 20α-hydroxy steroid dehydrogenase with decreased activity of delta5-3β-hydroxy steriod dehydrogenase and release of delta4-3-oxo steroids in vitro. 2. Similar effects of foetoplacental removal are noted in pregnant mice. 3. Gonadotrophin induced lower activities of 20α-hydroxy steroid dehydrogenase, except at the very end of pregnancy, and partly inhibited the induction caused by foetoplacental removal. 4. The results suggest that existence of a placental factor that restrains these changes until the end of normal pregnancy, which is produced in amounts proportional to the number of placentae and is conveyed to the ovary via the blood. 5. This factor was not replaced by prolactin. 6. It is argued that neither placental lactogen nor pituitary luteotrophin participate in the induction of 20α-hydroxy steroid dehydrogenase at late pregnancy in the rat. 7. Aminoglutethimide induced 20α-hydroxy steroid dehydrogenase only in late pregnancy. This was partly reversed by progesterone, wholly reversed by progesterone plus oestrogen, and did not involve the pituitary.

scholarly journals Inhibitory effect of leptin on the rat ovary during the ovulatory process

Reproduction ◽  
2006 ◽  
Vol 132 (5) ◽  
pp. 771-780 ◽  
Author(s):  
A G Ricci ◽  
M P Di Yorio ◽  
A G Faletti
Keyword(s):  
Leptin Receptor ◽  
Inhibitory Effect ◽  
Chorionic Gonadotrophin ◽  
Prostaglandin E ◽  
Negative Effects ◽  
Serum Progesterone ◽  
Leptin Receptors ◽  
The Media ◽  
Ovulatory Process

The aims of this study were to investigate the negative action of leptin on some intraovarian ovulatory mediators during the ovulatory process and to assess whether leptin is able to alter the expression of its ovarian receptors. Immature rats primed with gonadotrophins were used to induce ovulation. Serum leptin concentration was diminished 4 h after human chorionic gonadotrophin (hCG) administration, whereas the ovarian expression of leptin receptors, measured by western blot, was increased by the gonadotrophin treatment. Serum progesterone level, ovulation rate and ovarian prostaglandin E (PGE) content were reduced in rats primed with equine chorionic gonadotrophin (eCG)/hCG and treated with acute doses of leptin (five doses of 5 μg each). These inhibitory effects were confirmed by in vitro studies, where the presence of leptin reduced the concentrations of progesterone, PGE and nitrites in the media of both ovarian explants and preovulatory follicle cultures. We also investigated whether these negative effects were mediated by changes in the expression of the ovarian leptin receptors. Since leptin treatment did not alter the expression of ovarian leptin receptor, the inhibitory effect of leptin on the ovulatory process may not be mediated by changes in the expression of its receptors at ovarian level, at least at the concentrations assayed. In summary, the ovulatory process was significantly inhibited in response to an acute treatment with leptin, and this effect may be due, at least in part, to the direct or indirect impairment of some ovarian factors, such as prostaglandins and nitric oxide.

PROSTAGLANDIN PRODUCTION BY INTRA-UTERINE TISSUES FROM PERIPARTURIENT SHEEP: USE OF A SUPERFUSION TECHNIQUE

1978 ◽  
Vol 76 (1) ◽  
pp. 111-121 ◽  
Author(s):  
M. D. MITCHELL ◽  
A. P. F. FLINT
Keyword(s):  
Arachidonic Acid ◽  
Relative Rate ◽  
Prostaglandin E ◽  
Tissue Samples ◽  
Prostaglandin Production ◽  
Small Tissue ◽  
Prostaglandin F

SUMMARY A technique for the continuous superfusion of small tissue samples in vitro has been applied to the study of prostaglandin production by ovine intra-uterine tissues. Basal and oxytocin-stimulated production of prostaglandins was studied at 120–125 days of pregnancy and after dexamethasone-induced delivery. In general, the relative rate of prostaglandin production by tissues was: foetal cotyledon = maternal cotyledon>myometrium and in quantitative order the prostaglandins produced were prostaglandin E (PGE) > prostaglandin F (PGF) = 13,14-dihydro-15-oxo-prostaglandin F (PGFM). Considerable variation was found between the rates of prostaglandin production in individual sheep. Oxytocin had no effect on the production of prostaglandins by tissues obtained before labour but myometrium and maternal cotyledon obtained at delivery exhibited a significant increase in production of PGE and PGF (though not PGFM) in response to oxytocin. Administration of arachidonic acid increased the production of PGE and PGF by the foetal cotyledon.

Inhibition of cytochrome P-450 C17 enzyme by a GnRH agonist in ovarian follicles from gonadotropin-stimulated rats

2007 ◽  
Vol 292 (5) ◽  
pp. E1456-E1464 ◽  
Author(s):  
Griselda Irusta ◽  
Fernanda Parborell ◽  
Marta Tesone
Keyword(s):  
Direct Action ◽  
Regulatory Protein ◽  
Follicular Development ◽  
Inhibitory Effect ◽  
Female Rats ◽  
Serum Progesterone ◽  
Protein Levels ◽  
Androgen Synthesis ◽  
Cytochrome P 450

Our objective was to study the direct action of a GnRH-I agonist, leuprolide acetate (LA), on ovarian steroidogenesis in preovulatory follicles obtained from equine chorionic gonadotropin (eCG)-treated rats. Previously, we have demonstrated an inhibitory effect of LA on steroidogenesis and follicular development. In this study, we tested the hypothesis that gonadotropin-releasing hormone (GnRH) exerts its negative effect on follicular development by inhibiting thecal cytochrome P-450 C17 (P450C17) α-hydroxylase expression and, consequently, androgen synthesis. Studies were carried out in prepubertal female rats injected with either eCG (control) or eCG plus LA (LA) and killed at different time points. Immunohistochemical studies indicated that LA induced steroidogenic acute regulatory protein (StAR) expression mainly in theca cells of preantral and antral follicles. In addition, serum progesterone levels increased significantly ( P < 0.05), whereas those of androsterone decreased ( P < 0.05) after 8 h of LA treatment. This inhibition caused by LA seemed to be a consequence of the decreased expression of follicular P450C17 α-hydroxylase, as demonstrated by Western blot and RT-PCR techniques. In vitro studies using follicles isolated from 48-h-eCG-treated rats and cultured with LA showed a significant ( P < 0.05) inhibition of FSH-induced androsterone follicular content as well as P450C17 α-hydroxylase protein levels, as determined by Western analysis. However, LA increased StAR protein expression in these follicles without significant changes in P450scc enzyme levels. Taking all these findings into account, we suggest that GnRH-I exerts a direct inhibitory action on gonadotropin-induced follicular development by decreasing the temporal expression of the P450C17 enzyme and, consequently, androgen production, thus reducing the supply of estrogens available to developing follicles.

scholarly journals Autophagy Attenuation Hampers Progesterone Synthesis during the Development of Pregnant Corpus Luteum

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 71
Author(s):  
Zonghao Tang ◽  
Zhenghong Zhang ◽  
Hong Zhang ◽  
Yuhua Wang ◽  
Yan Zhang ◽  
...  
Keyword(s):  
Lipid Droplets ◽  
Mtor Signaling ◽  
Serum Progesterone ◽  
Pregnant Rats ◽  
Luteal Cells ◽  
Low Level ◽  
Progesterone Production ◽  
Progesterone Synthesis ◽  
Related Proteins

The contribution of autophagy to catabolic balance has been well-established in various types of cells, whereas the involvement of autophagy in progesterone synthesis during rat pregnancy still remains unknown. Therefore, the present study was designed to evaluate the role of autophagy in progesterone production during the luteal development of pregnant rats. The results showed autophagy-related proteins was maintained at a low level on day 10 after pregnancy, significantly induced on day 16 and subsided to a relative low level on day 21, which was consistent with the changes of serum progesterone levels. The findings further indicated the contribution of autophagy to progesterone production was regulated by inactivation of Akt/mTOR signaling during the luteal development of pregnant rats in in vivo and in vitro experiments. Further investigations revealed autophagy may be involved in the surge of progesterone production in pregnant rats, as inhibition of autophagy by 3-MA compromised serum progesterone levels. Furthermore, 3-MA treatment also leveled down the number of lipid droplets in luteal cells, implying that autophagy may affect the production of progesterone by manipulating the formation of lipid droplets in luteal cells. In addition, the results suggested that mitophagy was mobilized during the primary stage of luteolysis and inhibition of autophagy promoted the increase of redundant mitochondrial and cytoplasmic cytochrome C in luteal cells of pregnant rats. Taken together, the present study indicated that autophagy-related proteins were induced by the inactivation of Akt/mTOR signaling and then contributed to the progesterone production possibly by affecting the formation of intracellular lipid droplets during the luteal development of pregnant rats. To our knowledge, this will provide a new insight into the important mechanism of autophagy regulating progesterone production in ovaries of pregnant mammals.

Effect of Tumor Necrosis Factor-α on in vitro Prostaglandin Production in Buffalo Corpus Luteum

2021 ◽  
Author(s):  
M.K. Tripathi ◽  
S. Mondal ◽  
I.J. Reddy ◽  
A. Mor
Keyword(s):  
Mrna Expression ◽  
Corpus Luteum ◽  
Prostaglandin E ◽  
Prostaglandin F ◽  
Important Regulator ◽  
Factor Α ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Necrosis Factor

Background: Corpus luteum plays key role in embryonic survival. Prostaglandins are the important regulator controlling the life span of corpus luteum. The present study investigated the effect of various doses of TNFα on in vitro PGF2α and PGE2 production and expression profiling of PGFS and PGES mRNA in buffalo Corpus Luteum (CL).Methods: Buffalo ovaries with mid-luteal phase CL were collected from the abattoir and CL were enucleated from surrounding tissues. Corpus luteum were finely chopped, rinsed with HBSS (Hanks Balanced Salt Solution) medium; supplemented with gentamycin and 0.1% BSA and incubated at 37°C for 1 hr in HBSS containing 0.1% collagenase. The cell suspension following filtration was washed by HBBS supplemented with gentamycin and 0.1% BSA (bovine serum albumin) and was treated with increasing doses of TNFα (0.1, 0.5 and 1.0 nM) and cultured at 38.5°C, 5% CO2 level for 24 hr. Result: There was dose dependent increase in concentrations of PGF2α and PGE2 with increasing doses of TNFα. The PGFS (prostaglandin F synthase) mRNA expression increased with increasing doses of TNFα. However, there was decrease in PGES (prostaglandin E synthase) mRNA expression at 0.1 nM and 0.5 nM TNFα but PGES mRNA expression increased at 1.0 nM TNFα as compared to control. It can be concluded that TNFα may alter PGES and PGFS mRNA expression and prostaglandin secretion in buffalo CL. 

Abstract P639: Sildenafil Treatment Improves Placental Levels of Placental Growth Factor in the Dahl Salt-Sensitive Pregnant Rat Model of Superimposed Preeclampsia

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Ana C Palei ◽  
Jennifer M Sasser ◽  
Joey P Granger
Keyword(s):  
Growth Factor ◽  
Umbilical Vein ◽  
Resistance Index ◽  
Placental Growth Factor ◽  
Trophoblast Invasion ◽  
Maternal Circulation ◽  
Pregnant Rats ◽  
Pregnant Rat

Although the etiology of preeclampsia (PE) remains unclear, evidence indicates that impaired trophoblast invasion followed by placental ischemia promotes the release of placental anti-angiogenic factors into the maternal circulation. These factors then elicit maternal endothelial dysfunction and hypertension by blocking the action of molecules such as the placental growth factor (PlGF). Inhibition of phosphodiesterase (PDE)-5 with sildenafil or other has been proposed as a potential therapy for PE; however, the mechanisms whereby PDE-5 inhibitors reduce blood pressure (BP) and improve uteroplacental perfusion during pregnancy are not clear. While previous studies have shown that PDE-5 inhibition induces PlGF production from human umbilical vein endothelial cells; it is unknown whether PDE-5 inhibitors also increase PlGF from placenta. Thus, the aim of this study was to evaluate whether sildenafil enhance placental secretion/production of PlGF in vitro and in vivo. In our in vitro protocol, we incubated placental villous explants from Sprague Dawley (SD) pregnant rats (n=4, 2-3 placentas per rat) at gestational day (GD)19 with different doses of sildenafil for 48h at 37°C under normoxia (8% O 2 ). PlGF-2 was measured in media of cultured explants by ELISA. We observed that sildenafil had no effect on PlGF-2 secretion from rat placental villi (vehicle: 562.7±46.6, 10nM: 559.3±39.5, 100nM: 556.4±35.9, 10uM: 546.2±37.5, and 100uM: 558.7±48.2pg/mg; P>0.05). In our in vivo protocol, we treated Dahl Salt-Sensitive (DS) pregnant rats (n=6-8 per group), which we had previously characterized as a model of superimposed PE, with sildenafil (50mg/kg per day, via food) from GD10 to 20. PlGF-2 was measured in placental homogenates by ELISA. While untreated DS dams exhibited an increase in BP and uterine artery resistance index (UARI) from baseline to late pregnancy, sildenafil-treated DS dams exhibited a significant decrease in BP and UARI. In addition, we found that placental levels of PlGF-2 were elevated in sildenafil-treated DS dams compared with untreated counterparts (1019±107.3 and 646.8±125.1pg/mg; P=0.0407). In conclusion, our findings suggest that the BP and UARI reduction in response to sildenafil may involve the indirect production of PlGF.

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