Acth Levels in Amniotic Fluid During Pregnancy

Tuimala, Risto; Kauppila, Antti; Haapalahti, J.

doi:10.1111/j.1471-0528.1976.tb00759.x

Cited by 27 publications

(11 citation statements)

References 14 publications

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“…This rise of maternal ACTH levels is due to circulating unbound placental CRH. ACTH concentration in amniotic fluid rises during pregnancy, peaking at the beginning of the third trimester, and then showing a decline 68…”

Section: Maternal Hpa Axis In Pregnancymentioning

confidence: 99%

“…ACTH concentration in amniotic fluid rises during pregnancy, peaking at the beginning of the third trimester, and then showing a decline. 68 Elevated estrogen levels in pregnancy lead to a doubling of corticosteroidbinding globulin (CBG) levels, 66 resulting in low catabolism of cortisol by the liver and a doubling of cortisol's half-life in plasma. Moreover, during pregnancy maternal adrenal glands gradually become hypertrophic as cortisol production in the adrenal zona fasciculata is increased, because of the relatively increased maternal ACTH secretion.…”

Section: Maternal Hpa Axis In Pregnancymentioning

confidence: 99%

See 1 more Smart Citation

Maternal and Fetal Hypothalamic‐Pituitary‐Adrenal Axes During Pregnancy and Postpartum

Mastorakos

Ilias

2003

Annals of the New York Academy of Sciences

531

360

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The principal modulators of the hypothalamic-pituitary-adrenal (HPA) axis are corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP). Corticotropin-releasing hormone is not exclusively produced in the hypothalamus. Its presence has been demonstrated at peripheral inflammatory sites. Ovulation and luteolysis bear characteristics of an aseptic inflammation. CRH was found in the theca and stromal cells as well as in cells of the corpora lutea of human and rat ovaries. The cytoplasm of the glandular epithelial cells of the endometrium has been shown to contain CRH and the myometrium contains specific CRH receptors. It has been suggested that CRH of fetal and maternal origin regulates FasL production, thus affecting the invasion (implantation) process through a local auto-paracrine regulatory loop involving the cytotrophoblast cells. Thus, the latter may regulate their own apoptosis. During pregnancy, the plasma level of circulating maternal immunoreactive CRH increases exponentially from the first trimester of gestation due to the CRH production in the placenta, decidua, and fetal membranes. The presence in plasma and amniotic fluid of a CRH-binding protein (CRHbp) that reduces the bioactivity of circulating CRH by binding is unique to humans. Maternal pituitary ACTH secretion and plasma ACTH levels rise during pregnancy-though remaining within normal limits-paralleling the rise of plasma cortisol levels. The maternal adrenal glands during pregnancy gradually become hypertrophic. Pregnancy is a transient, but physiologic, period of hypercortisolism. The diurnal variation of plasma cortisol levels is maintained in pregnancy, probably due to the secretion of AVP from the parvicellular paraventricular nuclei. CRH is detected in the fetal hypothalamus as early as the 12th week of gestation. CRH levels in fetal plasma are 50% less than in maternal plasma. The circulating fetal CRH is almost exclusively of placental origin. The placenta secretes CRH at a slower rate in the fetal compartment. AVP is detected in some neurons of the fetal hypothalamus together with CRH. AVP is usually detectable in the human fetal neurohypophysis at 11 to 12 weeks gestation and increases over 1000-fold over the next 12 to 16 weeks. The role of fetal AVP is unclear. Labor appears to be a stimulus for AVP release by the fetus. The processing of POMC differs in the anterior and intermediate lobes of the fetal pituitary gland. Corticotropin (ACTH) is detectable by radioimmunoassay in fetal plasma at 12 weeks gestation. Concentrations are higher before 34 weeks gestation, with a significant fall in late gestation. The human fetal adrenal is enormous relative to that of the adult organ. Adrenal steroid synthesis is increased in the fetus. The major steroid produced by the fetal adrenal zone is sulfoconjugated dehydroepiandrosterone (DHEAS). The majority of cortisol present in the fetal circulation appears to be of maternal origin, at least in the nonhuman primate. The fetal adrenal uses the large amounts of progesterone supplied by th...

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Section: Maternal Hpa Axis In Pregnancymentioning

confidence: 99%

Section: Maternal Hpa Axis In Pregnancymentioning

confidence: 99%

Maternal and Fetal Hypothalamic‐Pituitary‐Adrenal Axes During Pregnancy and Postpartum

Mastorakos

Ilias

2003

Annals of the New York Academy of Sciences

531

360

View full text Add to dashboard Cite

show abstract

“…However, placental ACTH transfer from fetus to mother, or vice versa, does not occur (Winters et al . 1974; Tuimala et al . 1976).…”

Section: Production Of Pomc Derivatives In the Placentamentioning

confidence: 99%

“…In rats, the ACTH concentration in fetal plasma is higher (10-30 nM) than that in maternal plasma (undetectable level). However, placental ACTH transfer from fetus to mother, or vice versa, does not occur (Winters et al 1974;Tuimala et al 1976). Intriguingly, a surge of plasma ACTH levels in rat fetuses appears at 14 days post coitus (dpc) ( Fig.…”

Section: Production Of Pomc Derivatives In the Placentamentioning

confidence: 99%

Effects of melanocortins on fetal development

Simamura¹,

Shimada²,

Shoji

et al. 2011

Congenital Anomalies

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Melanocortins, adrenocorticotropic hormone (ACTH) and α-, β-, and γ-melanocyte-stimulating hormone (MSH) are produced in the placenta and secreted into embryos/fetuses. ACTH concentrations are higher in fetal plasma than in maternal plasma and peak at mid-gestation in rats, whereas ACTH production starts in the anterior lobe of the fetal pituitary at later stages. Melanocortin receptors (MC1-5R), receptors for ACTH and α-, β- and γ-MSH, are expressed in various adult organs. The specific function of these receptors has been well examined in the hypothalamic-pituitary-adrenocortical (HPA) axis and the HPA axis-like network in the skin, and anti-inflammatory effects for white blood cells have also been investigated. MC2R and/or MC5R are also expressed in the testis, lung, kidney, adrenal, liver, pancreas, brain and blood cells at different stages in mouse and rat embryos/fetuses. Melanocortins in embryos and fetuses promote maturation of the HPA axis and also contribute to the development of lung, testis, brain and blood cells. Recently, a unique ACTH function was revealed in fetuses: placental ACTH, which is secreted by the maternal leukemia inhibitory factor (LIF), and induces LIF secretion from fetal nucleated red blood cells. Finally, the maternal LIF-placental ACTH-fetal LIF signal relay regulates the LIF level and promotes neurogenesis in fetuses, which suggests that ACTH acts as a signal transducer or effector for fetal development in the maternal-fetal signal pathway.

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“…This rise in the maternal ACTH levels is due to circulating unbound placental CRH [3]. The ACTH concentration in amniotic fluid increases during pregnancy, peaking at the beginning of the third trimester, then exhibiting a decline [4].…”

Section: Introductionmentioning

confidence: 99%

Relationship between alteration of the peptide hormone levels and depression during the gestational period

Hiramoto¹,

Yamate²,

Kobayashi³

2014

Res J Endocrinol Metab

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Background: Stress is considered to be a major factor in the development of depressive illness. Pregnancy is also a kind of physical stress, and the rate of pregnancy-induced depression is increasing. This study analyzed alterationsin the levels of peptide hormones in the gestational period in order to evaluate the prevalence of a depressed state during pregnancy. Methods: Specific pathogen-free C57BL/6j gestation female mice were used for the experiments. In order to investigate the prevalence of a depressed state in the gestational period, we conducted forced swim test (FST) and open field test (OFT) and measured the levels of plasma adrenocorticotropic hormone (ACTH), β-endorphin (β-End), corticosterone and dopamine (DA) in the gestational period. In addition, we measured the expression of prohormone convertase 2 (PC2) in the pituitary gland. Results: In the FST, the akinesia time (floating time) during the gestational period was the longest on gestational day (gd) 6, then gradually decreasd toward parturition. On the other hand, in the OFT, the motor activity during the gestational period increased gradually to gd 17 after being the lowest on gd 6. The plasma levels of ACTH and corticosterone fell gradually to gd 18 after a peak on gd 6. In contrast, the plasma levels of β-End and DA and the expression of PC2 in the pituitary gland increased throughout the gestational period, peaking by gd 18. Conclusions: These observations suggest that the levels of ACTH and corticosterone change in parallel with those of β-End and DA during the gestational period and function to regulate a depressed state.

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Acth Levels in Amniotic Fluid During Pregnancy

Cited by 27 publications

References 14 publications

Maternal and Fetal Hypothalamic‐Pituitary‐Adrenal Axes During Pregnancy and Postpartum

Maternal and Fetal Hypothalamic‐Pituitary‐Adrenal Axes During Pregnancy and Postpartum

Effects of melanocortins on fetal development

Relationship between alteration of the peptide hormone levels and depression during the gestational period

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