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 A proposed sequence of hormones controlling the induction of luteal 20α-hydroxy steroid dehydrogenase and progesterone withdrawal in the late-pregnant rat

1976 ◽  
Vol 160 (3) ◽  
pp. 663-670 ◽  
Author(s):  
D H Smith ◽  
N J Kuhn
Keyword(s):  
Follicle Stimulating Hormone ◽  
Late Pregnancy ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Human Choriogonadotropin ◽  
Pregnant Mare Serum Gonadotropin ◽  
Progesterone Synthesis ◽  
Serum Gonadotropin ◽  
Hydroxy Steroid ◽  
Steroid Dehydrogenase

1. The previously reported induction of luteal 20α-hydroxy steroid dehydrogenase by administration of aminoglutethimide to late-pregnant rats was shown to be unaffected by prior removal of the foetuses. Aminoglutethimide therefore does not act via the foetuses in this context. 2. The ability of injected oestrogen to prevent the above induction was lost by delaying the injection for 12h after aminoglutethimide, although the increase in enzyme activity begins only after 24h. 3. Induction of 20α-hydroxy steroid dehydrogenase by foetoplacental removal on day 18 of pregnancy was inhibited by human choriogonadotropin, lutropin (luteinizing hormone) and pregnant-mare serum gonadotropin, but not by somatotropin (growth hormone), thyrotropin or follitropin (follicle-stimulating hormone) 4. Indomethacin blocked the normal induction of 20α-hydroxy steroid dehydrogenase in late pregnancy and that caused by aminoglutethimide. It partially blocked that caused by human choriogonadotropin given on days 19-20 and that caused by 2-bromo-α-ergocryptine on days 5-6, but failed to block that caused by human choriogonadotropin on days 15-16 or by foetoplacental removal on day 18 of pregnancy. 5. These findings, and the control of progesterone synthesis in late pregnancy, are interpreted in terms of a sequence of hormonal or enzymic syntheses, each of which is inhibited by the product of the preceding synthesis.

scholarly journals Maximal expression of suppressors of cytokine signaling in the rat ovary occurs in late pregnancy

Reproduction ◽  
2009 ◽  
Vol 138 (3) ◽  
pp. 537-544 ◽  
Author(s):  
Stephen T Anderson ◽  
Naajia N M Isa ◽  
Johanna L Barclay ◽  
Michael J Waters ◽  
Jon D Curlewis
Keyword(s):  
Mrna Expression ◽  
Prolactin Receptor ◽  
Prostaglandin F2α ◽  
Late Pregnancy ◽  
Placental Lactogen ◽  
Cytokine Signaling ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Rat Ovary ◽  
Suppressors Of Cytokine Signaling

Maintenance of the rodent corpus luteum (CL) during pregnancy requires prolactin receptor (PRLR) signal transduction via STAT5. At the end of pregnancy, prostaglandin F2α (PGF2α) induces luteal regression through many mechanisms, including downregulation of PRLR signaling. We have previously shown that a PGF2α analog upregulates suppressors of cytokine signaling (SOCS) proteins in the CL of day 19 pregnant rats leading to reduced STAT5 signaling. Here, we examined endogenous SOCS expression and STAT5 signaling in the rat ovary during normal pregnancy and luteolysis. The mRNA expression of Socs1, Socs2, and Socs3 and related cytokine-inducible SH2-containing protein (Cish) was low in early pregnancy (day 7), but significantly increased at mid-pregnancy (days 10 and 13) associated with increased endogenous tyrosine phosphorylation (TyrP) of STAT5. In support of the notion that these changes are due to increasing placental lactogen levels at this time, we found that treatment with exogenous PRL on day 7 increased TyrP of STAT5 and induced SOCS mRNA expression, except Socs3. After mid-pregnancy, further significant increases in Socs3 and Cish mRNA expression were observed. Such changes in mRNA expression correlated with protein levels, with protein levels of both SOCS3 and CISH being maximal in late pregnancy (days 19–21). In addition, a significant reduction in TyrP of STAT5 was first observed on day 20, with a further substantial decrease on day 21. Therefore, these results are consistent with the hypothesis that increased SOCS expression in the rat ovary during late pregnancy reduces STAT5 signaling, which may be important in PGF2α-induced luteolysis.

MORPHOLOGICAL CHANGES IN THE ENDOCRINE PANCREAS IN PREGNANT RATS WITH EXPERIMENTAL DIABETES

1979 ◽  
Vol 80 (2) ◽  
pp. 175-179 ◽  
Author(s):  
F. A. VAN ASSCHE ◽  
L. AERTS ◽  
W. GEPTS
Keyword(s):  
Endocrine Pancreas ◽  
Experimental Diabetes ◽  
Morphological Changes ◽  
Normal Pregnancy ◽  
Β Cells ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Human Pregnancy ◽  
The Individual

This present study has demonstrated that during normal pregnancy in the rat the number of β-cells is increased (hyperplasia) and the volume of the individual β-cells is increased (hypertrophy). During experimental diabetes, however, the endocrine pancreas has an impaired capacity to compensate during pregnancy. In the experimental diabetic pregnant rat the β-cells cannot replicate due to the unfavourable metabolic environment. This could reflect the complications caused by diabetes during human pregnancy.

Hyperlipemia and ketosis in the pregnant rat

1964 ◽  
Vol 206 (4) ◽  
pp. 796-804 ◽  
Author(s):  
Robert O. Scow ◽  
Sidney S. Chernick ◽  
Marlene S. Brinley
Keyword(s):  
Blood Glucose Concentration ◽  
Late Pregnancy ◽  
Maternal Blood ◽  
Insulin Administration ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Fat Mobilization ◽  
Fractional Clearance ◽  
Ad Libitum ◽  
Fasted Rats

Pregnant rats fasted on the 18th or 19th day of gestation developed hypoglycemia, severe ketosis, and hyperlipemia. The latter, which consisted primarily of triglycerides, was accompanied by increased plasma free fatty acids and accumulation of fat in the liver and kidneys. The effects of fasting were diminished by starting the fast earlier in pregnancy or by hysterectomy. Both ketosis and hyperlipemia were corrected by administration of insulin, tolbutamide, or glucose. The findings indicate that increased fat mobilization and ketosis in fasting pregnant rats are the result of insulin lack. It is suggested that the high priority of the fetuses for glucose reduced the maternal blood glucose concentration to a level too low to stimulate insulin secretion during fasting. Fasting did not alter the rapid growth of the fetuses. Pregnant rats fed ad libitum also developed hypertriglyceridemia if the diet contained fat. This hyperlipemia, unlike that in the fasted rats, was not due to increased fat mobilization and was unaffected by insulin administration. It is concluded that the fractional clearance of blood triglycerides is greatly reduced during late pregnancy.

PLASMA AND PITUITARY LUTEINIZING HORMONE CONCENTRATIONS AND PERIPHERAL PLASMA OESTRADIOL CONCENTRATION DURING EARLY PREGNANCY AND AFTER THE ADMINISTRATION OF PROGESTATIONAL STEROIDS IN THE RAT

1972 ◽  
Vol 53 (1) ◽  
pp. 31-35 ◽  
Author(s):  
K. BROWN-GRANT ◽  
C. S. CORKER ◽  
F. NAFTOLIN
Keyword(s):  
Luteinizing Hormone ◽  
Marked Decrease ◽  
Single Injection ◽  
Normal Pregnancy ◽  
Oestrous Cycle ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Peripheral Plasma ◽  
Blastocyst Implantation ◽  
Plasma Oestradiol

SUMMARY Plasma luteinizing hormone (LH) concentrations were already lower on Day 2 of pregnancy than at the same time after the preceding ovulation in the non-pregnant rat, and fell progressively up to Day 16 of pregnancy. No evidence was obtained of any increase at the time when the ovulatory surge of LH would have occurred if the animal had not become pregnant. Pituitary LH concentration was lower in mated rats on the morning of Day 0 of pregnancy than in unmated controls on the morning of the day of oestrus. Subsequently it increased slowly to reach a level higher than at any stage of the oestrous cycle by Day 8 of pregnancy and remained high until at least Day 16 of pregnancy. Peripheral plasma oestradiol concentration increased late on Day 2 of pregnancy and was still raised on Day 4 but was never more than about one fourth of the peak concentration seen on the morning of prooestrus during the oestrous cycle. There were similar changes in plasma LH and oestradiol concentrations in the 48 h after a single injection of 2·5mg progesterone on the morning of the day of dioestrus, a procedure that delays ovulation by 1 or 2 days. Administration of a synthetic progestational compound (medroxyprogesterone acetate) to pregnant rats delayed blastocyst implantation and the delay was associated with a marked decrease in peripheral plasma LH to levels below those of normal pregnancy.

Possible role of gap junctions in activation of myometrium during parturition

1978 ◽  
Vol 235 (5) ◽  
pp. C168-C179 ◽  
Author(s):  
R. E. Garfield ◽  
S. M. Sims ◽  
M. S. Kannan ◽  
E. E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Gap Junctions ◽  
Freeze Fracture ◽  
Normal Pregnancy ◽  
Pregnant Rats ◽  
Junction Formation ◽  
Synchronous Contraction ◽  
Do So

Gap junctions between smooth muscle cells of the myometrium of pregnant rats were found only immediately prior to, during and immediately after parturition by quantitative thin-section and freeze-fracture microscopy. Ovariectomy of 16- to 17-days-pregnant rats resulted in premature termination of pregnancy and the appearance of gap junctions. Methods that prolonged normal pregnancy in rats or maintained pregnancy in ovariectomized animals (progesterone treatment) prevented the appearance of gap junctions. Gap junctions formed in tissues incubated for 24--96 h in vitro without any hormonal influence. We propose that gap junctions are essential for normal labor and delivery for synchronous contraction of the muscle of the uterus. We present a model for control of parturition that may apply to other animals including humans. The model proposes: 1) the possible roles progesterone, prostaglandins, or estrogens may play in initiating gap-junction formation; 2) that the formation of gap junctions is a necessary step in activation of the myometrium leading to labor; and 3) that agents used to stimulate or inhibit labor may do so by affecting gap junctions.

scholarly journals Increased renal α-epithelial sodium channel (ENAC) protein and increased ENAC activity in normal pregnancy

2010 ◽  
Vol 299 (5) ◽  
pp. R1326-R1332 ◽  
Author(s):  
Crystal West ◽  
Zheng Zhang ◽  
Geoffrey Ecker ◽  
Shyama M. E. Masilamani
Keyword(s):  
Plasma Volume ◽  
Late Pregnancy ◽  
Normal Pregnancy ◽  
In Vivo Studies ◽  
Volume Status ◽  
Plasma Volume Expansion ◽  
Pregnant Rats ◽  
Mineralocorticoid Receptor Antagonist ◽  
The Difference

Pregnancy-mediated sodium (Na) retention is required to provide an increase in plasma volume for the growing fetus. The mechanisms responsible for this Na retention are not clear. We first used a targeted proteomics approach and found that there were no changes in the protein abundance compared with virgin rats of the β or γ ENaC, type 3 Na+/H+ exchanger (NHE3), bumetanide-sensitive cotransporter (NKCC2), or NaCl cotransporter (NCC) in mid- or late pregnancy. In contrast, we observed marked increases in the abundance of the α-ENaC subunit. The plasma volume increased progressively during pregnancy with the greatest plasma volume being evident in late pregnancy. ENaC inhibition abolished the difference in plasma volume status between virgin and pregnant rats. To determine the in vivo activity of ENaC, we conducted in vivo studies of rats in late pregnancy ( days 18–20) and virgin rats to measure the natriuretic response to ENaC blockade (with benzamil). The in vivo activity of ENaC (UNaV postbenzamil-UNaV postvehicle) was markedly increased in late pregnancy, and this difference was abolished by pretreatment with the mineralocorticoid receptor antagonist, eplerenone. These findings demonstrate that the increased α-ENaC subunit of pregnancy is associated with an mineralocorticoid-dependent increase in ENaC activity. Further, we show that ENaC activity is a major contributor of plasma volume status in late pregnancy. These changes are likely to contribute to the renal sodium retention and plasma volume expansion required for an optimal pregnancy.

scholarly journals Assessment of Cytotoxicity, Fetotoxicity, and Teratogenicity ofPlathymenia reticulataBenth Barks Aqueous Extract

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Lia de Barros Leite Albuquerque ◽  
Cháriston André Dal Belo ◽  
Marcio Galdino dos Santos ◽  
Patricia Santos Lopes ◽  
Marli Gerenutti ◽  
...  
Keyword(s):  
Aqueous Extract ◽  
Reproductive Toxicity ◽  
Late Pregnancy ◽  
Control Group ◽  
Corpora Lutea ◽  
Experimental Conditions ◽  
Pregnant Rats ◽  
Skeletal Analysis ◽  
Ld50 Test

Scientific assessment of harmful interactions of chemicals over the entire reproductive cycle are divided into three segments based on the period: from premating and mating to implantation (I), from implantation to major organogenesis (II), and late pregnancy and postnatal development (III). We combined the segments I and II to assessPlathymenia reticulataaqueous extract safety. In order to investigate reproductive toxicity (segment I), pregnant rats received orally 0.5 or 1.0 g/kg of extract, daily, during 18 days. These concentrations were determined by a preliminaryin vitroLD50 test in CHO-k1 cells. A control group received deionized water. The offspring was removed at the 19th day, by caesarean, and a teratology study (segment II) was carried out. The corpora lutea, implants, resorptions, live, and dead fetuses were then counted. Placenta and fetuses were weighted. External and visceral morphology were provided by the fixation of fetuses in Bouin, whereas skeletal analysis was carried out on the diaphanizated ones. The increase in the weights of placenta and fetuses was the only abnormality observed. Since there was no sign of alteration on reproduction parameters at our experimental conditions, we conclude thatP. reticulataaqueous extract is safe at 0.5 to 1.0 g/kg and is not considered teratogenic.

EFFECTS OF INJECTIONS OF MONOAMINE OXIDASE INHIBITOR OR SALINE INTO THE UTERUS IN LATE PREGNANCY ON UTERINE CATECHOLAMINE LEVELS RELATED TO ABNORMAL PARTURITION IN RATS

1975 ◽  
Vol 67 (3) ◽  
pp. 371-383 ◽  
Author(s):  
J. P. MALTIER ◽  
F. CAVAILLE
Keyword(s):  
Monoamine Oxidase ◽  
Monoamine Oxidase Inhibitor ◽  
Late Pregnancy ◽  
Ringer Solution ◽  
Oxidase Inhibitor ◽  
Saline Injection ◽  
Mao Inhibitor ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Catecholamine Levels

SUMMARY Injection of a monoamine oxidase (MAO) inhibitor (nialamide) into the uterus of an anaesthetized and laparotomized rat on day 20 of pregnancy severely disturbed parturition. Injection of the solvent (0·9% isotonic NaCl solution) at the same stage of gestation produced the same but less frequent disturbances. When the rats were injected on days 19 or 21, impairment was less marked than on day 20. Therefore, day 20 seems to be a critical period for the onset of parturition. Injection of Ringer solution into the uterus on day 20 had effects analogous to those of saline injection at the same stage. Anaesthesia induced with ether, laparotomy of the pregnant rat on day 20, and handling of the uterine horns without injection of either Ringer or NaCl also disturbed parturition in 70% of the rats treated. Nevertheless, disorders were not as severe as those after injection. Laparotomy alone on day 20 did not disturb parturition. The effects on parturition of a saline injection into the uterus on day 20 were greatly decreased when the injection was performed on pregnant rats adrenalectomized on day 14, or on pregnant rats pretreated on days 18 and 19 with an agent blocking the adrenergic β receptors (propranolol); 70–80% of the treated rats had normal deliveries. In control rats, uterine catecholamine levels were markedly modified between days 21 and 22 of gestation. These changes did not occur in rats injected with MAO inhibitor or saline.

Pregnancy Does Not Increase Susceptibility to Bupivacaine in Spinal Root Axons

1997 ◽  
Vol 87 (3) ◽  
pp. 610-616 ◽  
Author(s):  
Friederike B. Dietz ◽  
Richard A. Jaffe
Keyword(s):  
Conduction Block ◽  
Late Pregnancy ◽  
Underlying Mechanism ◽  
Ventral Root ◽  
Spinal Root ◽  
Pregnant Rats ◽  
C Fibers ◽  
Antinociceptive Effects ◽  
The Difference

Background The underlying mechanism of enhanced antinociceptive effects and increased susceptibility to local anesthetics during pregnancy is not known. Mechanical, hormonal, biochemical, and neural changes have been suggested. The authors measured the susceptibility of individual spinal root axons to bupivacaine during late pregnancy in rats and compared them with similar measurements in nonpregnant rats. Methods Lumbar dorsal and ventral roots were excised from anesthetized pregnant and nonpregnant rats. Single-fiber dissection and recording techniques were used to isolate activity in individual axons. Supramaximal constant voltage stimuli were delivered to the distal end of the root. During in vitro perfusion, each root was exposed to increasing concentrations of bupivacaine, and the minimum blocking concentration (Cm) and the concentration that increased conduction latency by 50% (EC50) were measured. Results Myelinated and unmyelinated dorsal and ventral root axons of pregnant rats appeared to be less sensitive to steady-state conduction block and to the latency-increasing effects of bupivacaine than were equivalent axons from nonpregnant rats. Although when comparing specific axon types, only the difference in C-fibers was significant (Cm = 29.8 microM for pregnant and Cm = 22.1 microM for nonpregnant rats, P < 0.05; EC50 = 19.9 microM and 13.6 microM, respectively). Conclusions In contrast to clinical expectations, the susceptibility to bupivacaine conduction block in individual dorsal and ventral root axons during late pregnancy in rats was not greater in pregnant animals. Pregnancy-related changes in diffusion barriers and activation of endogenous analgesic systems without changes in the electrophysiologic properties of spinal root axons are suggested as possible explanations for the discrepancy between clinical and experimental observations.

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