Effect of adrenalectomy at different pregnancy stages on maternal and fetal serum corticosteroid binding globulin and corticosterone in the rat

1990 ◽  
Vol 122 (1) ◽  
pp. 121-126 ◽  
Author(s):  
Alia Cohen ◽  
Lia Savu ◽  
Roger Vranckx ◽  
Michelle Maya ◽  
Emmanuel A. Nunez
Keyword(s):  
Adrenal Glands ◽  
Late Pregnancy ◽  
Maternal Serum ◽  
Maternal Response ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Serum Corticosterone ◽  
Corticosteroid Binding Globulin ◽  
Fetal Serum ◽  
Adrenal Secretion

Abstract The response of pregnant rat corticosteroid binding globulin to maternal adrenalectomy was studied as a function of the stage of pregnancy. Non-pregnant or pregnant rats were deprived of their adrenal glands during 4 days. In non-pregnant animals, adrenalectomy led to undetectable corticosterone levels and to the doubling of corticosteroid binding globulin. In pregnant rats adrenalectomized at 12 days and studied at 16 days, the serum corticosterone was likewise undetectable and the corticosteroid binding globulin was doubled as compared with pregnant rats of the corresponding age. In contrast, adrenalectomy from day 14 to 18 or from day 16 to 20 did not deplete the maternal serum corticosterone and the corticosteroid binding globulin remained unchanged. Under these conditions neither fetal corticosteroid binding globulin nor fetal corticosterone were modified. However, when the pregnant rats adrenalectomized from day 16 to 20 also received an injection of 30 mg of metyrapone on days 19 and 20 in order to inhibit fetal adrenal secretion, the maternal response was again a depletion of serum corticosterone together with an increase in corticosteroid binding globulin. Under these conditions, the fetus also reacted by a fall of corticosterone and a rise of corticosteroid binding globulin. Our results suggest that the maternal response of corticosteroid binding globulin to adrenalectomy depends on the pregnancy stage inasmuch as it may be influenced by a supply of corticosterone from the fetus during late pregnancy. Moreover, they show that in this late period, fetal corticosteroid binding globulin is regulated independently.

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.

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.

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.

Production of slow α2-globulin in the pregnant rat

1977 ◽  
Vol 55 (3) ◽  
pp. 496-507 ◽  
Author(s):  
Margaret Kirkcaldy ◽  
George H. Beaton
Keyword(s):  
Molecular Weight ◽  
Fetal Liver ◽  
Maternal Serum ◽  
Amino Acid Incorporation ◽  
Immunofluorescent Localization ◽  
Rat Serum ◽  
Pregnant Rat ◽  
Acid Incorporation ◽  
Fetal Serum ◽  
Initial Source

Slow α2-globulin (Sα2G), a high molecular weight glycoprotein, appears as a component of rat serum in a wide variety of both physiologic and pathologic conditions, including pregnancy; it is also present in the neonate. In the present study, the protein was detectable in serum after 6 to 10 days, and was present at moderate levels on day 13, and thereafter through the rest of pregnancy. From immunofluorescent localization and 14C-labelled amino acid incorporation studies, sα2G was found to be localized in uterine and placental tissues and to be synthesized by these tissues as early as day 6 of gestation. Production continued throughout pregnancy. Synthesis in the liver of the pregnant rat began at day 17 of gestation, which is in contrast with the observation in pathologic conditions that liver synthesis is an initial source of the serum protein; substantial fetal liver synthesis was occurring at day 21 of gestation, and the amount in fetal serum was four times greater than that in maternal serum at that time. It is likely that the fetal liver produces sα2G as soon as it begins to function.

CONCENTRATION OF TRANSCORTIN IN THE PREGNANT RAT AND ITS FOETUSES

1977 ◽  
Vol 75 (3) ◽  
pp. 427-431 ◽  
Author(s):  
H. VAN BAELEN ◽  
G. VANDOREN ◽  
P. DE MOOR
Keyword(s):  
Maternal Serum ◽  
Radial Immunodiffusion ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Single Radial Immunodiffusion

The concentration of transcortin in serum from foetal, neonatal, pregnant and lactating rats was measured by a single radial immunodiffusion method. A decrease in transcortin concentration in sera from foetuses and pregnant rats occurred starting on days 19 and 20 of pregnancy respectively. A more pronounced fall in transcortin concentration in foetal and maternal serum was observed after treating pregnant rats with dexamethasone. These results suggest that corticosterone may be responsible for the observed changes in transcortin concentration.

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.

A profound decrease in maternal arginine uptake provokes endothelial nitration in the pregnant rat

2008 ◽  
Vol 294 (3) ◽  
pp. H1156-H1163 ◽  
Author(s):  
Ran Reshef ◽  
Doron Schwartz ◽  
Merav Ingbir ◽  
Alexander Shtabsky ◽  
Tamara Chernichovski ◽  
...  
Keyword(s):  
Northern Blot Analysis ◽  
Late Pregnancy ◽  
Endothelial Damage ◽  
Mrna Levels ◽  
Protein Nitration ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Cationic Amino Acid ◽  
Kinase C ◽  
Arginine Uptake

While a specific role for nitric oxide (NO) in inducing the hemodynamic alterations of pregnancy is somewhat controversial, it is widely accepted that excess NO is generated during pregnancy. l-Arginine is the sole precursor for NO biosynthesis. Among several transporters that mediate l-arginine uptake, cationic amino acid transporter-1 (CAT-1) acts as the specific arginine transporter for endothelial NO synthase. The present study was designed to test the hypothesis that, during pregnancy, when arginine consumption by the fetus is significantly increased, compensatory changes in maternal arginine uptake affect the endothelium. Uptake of radiolabeled arginine (l-[3H]arginine) by freshly harvested maternal aortic rings from pregnant rats decreased by 65 and 30% in mid- and late pregnancy, respectively, compared with those obtained from virgin animals. This decrease was associated with a significant increase in endothelial protein nitration (the footprint of peroxynitrite generation), as shown by both Western blotting and immunohistochemistry utilizing anti-nitrotyrosine antibodies, reflecting endothelial damage. Northern blot analysis revealed that steady-state aortic CAT-1 mRNA levels did not change throughout pregnancy, whereas CAT-1 protein abundance was significantly increased, peaking at mid-pregnancy. Protein content of protein kinase C (PKC)-α, which was previously shown to decrease CAT-1 activity, increased significantly in the pregnant animals and was associated with a significant increase in CAT-1 phosphorylation. Intraperitoneal injection of α-tocopherol, a PKC-α inhibitor, prevented the decrease in arginine transport and attenuated protein nitration. In conclusion, aortic arginine uptake is reduced during pregnancy, through posttranslational modulation of CAT-1 protein, presumably via upregulation of PKC-α. The aforementioned findings are associated with an increase in protein nitration and, therefore, in selected individuals, may lead to the development of certain forms of endothelial dysfunction, like preeclampsia.

scholarly journals Renal and colonic potassium transporters in the pregnant rat

2018 ◽  
Vol 314 (2) ◽  
pp. F251-F259 ◽  
Author(s):  
Crystal A. West ◽  
Paul A. Welling ◽  
David A. West ◽  
Richard A. Coleman ◽  
Kit-Yan Cheng ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Late Pregnancy ◽  
Distal Colon ◽  
Protein Abundance ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Collecting Ducts ◽  
Potassium Secretion ◽  
Potassium Retention

Gestational potassium retention, most of which occurs during late pregnancy, is essential for fetal development. The purpose of this study was to examine mechanisms underlying changes in potassium handling by the kidney and colon in pregnancy. We found that potassium intake and renal excretion increased in late pregnancy while fecal potassium excretion remained unchanged and that pregnant rats exhibited net potassium retention. By quantitative PCR we found markedly increased H+-K+-ATPase type 2 (HKA2) mRNA expression in the cortex and outer medullary of late pregnant vs. virgin. Renal outer medullary potassium channel (ROMK) mRNA was unchanged in the cortex, but apical ROMK abundance (by immunofluorescence) was decreased in pregnant vs. virgin in the distal convoluted tubule (DCT) and connecting tubule (CNT). Big potassium-α (BKα) channel-α protein abundance in intercalated cells in the cortex and outer medullary collecting ducts (by immunohistochemistry) fell in late pregnancy. In the distal colon we found increased HKA2 mRNA and protein abundance (Western blot) and decreased BKα protein with no observed changes in mRNA. Therefore, the potassium retention of pregnancy is likely to be due to increased collecting duct potassium reabsorption (via increased HKA2), decreased potassium secretion (via decreased ROMK and BK), as well as increased colonic reabsorption via HKA2.

scholarly journals Renal NCC is unchanged in the midpregnant rat and decreased in the late pregnant rat despite avid renal Na+ retention

2015 ◽  
Vol 309 (1) ◽  
pp. F63-F70 ◽  
Author(s):  
Crystal A. West ◽  
Alicia A. McDonough ◽  
Shyama M. E. Masilamani ◽  
Jill W. Verlander ◽  
Chris Baylis
Keyword(s):  
Mrna Expression ◽  
Regional Differences ◽  
Late Pregnancy ◽  
Kidney Cortex ◽  
Apical Region ◽  
Plasma Volume Expansion ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Apical Localization ◽  
In Pregnancy

Pregnancy is characterized by plasma volume expansion due to Na+ retention, driven by aldosterone. The aldosterone-responsive epithelial Na+ channel is activated in the kidney in pregnancy. In the present study, we investigated the aldosterone-responsive Na+-Cl− cotransporter (NCC) in mid- and late pregnant rats compared with virgin rats. We determined the abundance of total NCC, phosphorylated NCC (pNCC; pT53, pS71 and pS89), phosphorylated STE20/SPS-1-related proline-alanine-rich protein kinase (pSPAK; pS373), and phosphorylated oxidative stress-related kinase (pOSR1; pS325) in the kidney cortex. We also measured mRNA expression of NCC and members of the SPAK/NCC regulatory kinase network, serum and glucocorticoid-regulated kinase (SGK)1, total with no lysine kinase (WNK)1, WNK3, and WNK4. Additionally, we performed immunohistochemistry for NCC kidneys from virgin and pregnant rats. Total NCC, pNCC, and pSPAK/OSR1 abundance were unchanged in midpregnant versus virgin rats. In late pregnant versus virgin rats, total NCC and pNCC were decreased; however, pSPAK/OSR1 was unchanged. We detected no differences in mRNA expression of NCC, SGK1, total WNK1, WNK3, and WNK4. By immunohistochemistry, NCC was mainly localized to the apical region in virgin rats, and density in the apical region was reduced in late pregnancy. Therefore, despite high circulating aldosterone levels in pregnancy, the aldosterone-responsive transporter NCC is not increased in total or activated (phosphorylated) abundance or in apical localization in midpregnant rats, and all are reduced in late pregnancy. This contrasts to the mineralocorticoid-mediated activation of the epithelial Na+ channel, which we have previously reported. Why and how NCC escapes aldosterone activation in pregnancy is not clear but may relate to regional differences in aldosterone sensitivity the increased K+ intake or other undefined mechanisms.

Endothelium and aortic contraction to endothelin-1 in the pregnant rat

2000 ◽  
Vol 78 (5) ◽  
pp. 372-377 ◽  
Author(s):  
Amadou Moctar Dièye ◽  
Alexis Gairard
Keyword(s):  
Receptor Antagonist ◽  
Late Pregnancy ◽  
Female Rats ◽  
Pregnant Rats ◽  
Pregnant Rat ◽  
Endothelin 1 ◽  
Key Words Endothelin ◽  
Vasoconstrictor Peptide ◽  
Aortic Contraction

Endothelium-derived factors modulate tone and may be involved in hyporeactivity to vasoconstrictors, such as norepinephrine or angiotensin II, as has been previously described during gestation. The endothelium produces endothelin-1, a major vasoconstrictor peptide, therefore aortic contractions to endothelin-1 (10-10 to 3 ×10-7 M) were used to assess the role of the endothelium in pregnant Wistar rats (at 20 days of gestation). Late pregnancy is characterized by a significantly diminished systolic blood pressure in conscious rats (-17 mmHg, P < 0.001, n = 14). In pregnant and in age-matched nonpregnant female rats, endothelin-1 induced aortic contraction was greater when endothelium was present (at least P < 0.01). Indomethacin significantly reduced this contraction in aortic rings with intact endothelium in all groups. In aortic rings that had endothelium physically removed, contraction to endothelin-1 was greater in pregnant rats than in nonpregnant ones. Indomethacin decreased contraction of aortic rings in pregnant rats only. These results suggest an enhanced synthesis of vasoconstrictors by cyclooxygenases in vascular smooth muscle during pregnancy. In vessels with intact endothelium, we did not find hyporeactivity to endothelin-1 during late pregnancy. Contraction to endothelin-1 involved ETA receptors because it was decreased by BQ-123, an ETA receptor antagonist, whereas there was no significant change when using BQ-788, an ETB receptor antagonist. Key words: endothelin-1, endothelium, contraction, aorta, gestation.

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