Maternal-fetal endocrine interrelations: influence of maternal adrenocorticosteroids on fetal ACTH secretion

D'Angelo, SA; Paul, D. H.; Wall, N. R.

doi:10.1152/ajplegacy.1973.224.3.543

Cited by 18 publications

(7 citation statements)

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“…A slight increase during the last hours of in trauterine life is followed by a rapid decrease between hours 2 and 4. These results are con sistent with previous data on the decrease of adrenal weight between birth and the first 2 days of life (4,7,11). The adrenals have a hyperhemic appearance at birth whichdisappears by 4 h, suggesting that the glands were strongly stimulated.…”

Section: Adrenal Weightsupporting

confidence: 91%

“…This evolution, which reflects high fetal adrenal cortex activity at the moment of birth, is in agreement with the observed depletion of adrenal ascorbic acid as well as with the increase of the circulating cor ticosterone level. Although rat adrenal cor ticosterone evolution has already been de scribed during the perinatal period (7,17), the abrupt elevation of the glandular level of this hormone has not, to the best of our knowledge, been observed at the moment of birth. In addition, the decrease of the adrenal cor ticosterone level in 5-hour-old animals indicates a significant decrease of the synthetic capacity of these glands.…”

Section: Adrenal Corticosteronementioning

confidence: 90%

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Increased Adrenocortical Activity in the Newborn Rat

Corbier¹,

Roffi²

1978

Neonatology

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The evolution of adrenal weight, of the level of ascorbic acid and the levels of adrenal and plasma corticosterone were measured in the newborn rat at the moment of birth and during the hours that followed. Between 0 and 4 h, the absolute and relative weights of the adrenals decreased by 14 and 10%, respectively, and were even lower at 24 h. The amount of ascorbic acid in the adrenals decreases by 17% between 0 and 4 hours. Adrenal corticosterone levels dropped abruptly during the first hour of life, accompanied by an increase in the plasma levels of this hormone. These results suggest that during the initial hours of life, there is a significant stimulation of the adrenal cortex, probably connected to birth-related stress phenomena. An encephalectomy, leaving the pituitary in situ, or decapitation of the rat fetus during the last days of gestation impair the growth and endocrine activity of the adrenal glands. Normal adrenocortical function is restored by injecting hypothalamic extracts or ACTH at the time of surgery (9, 16). At the end of the gestation period, rat fetuses respond to such stimuli as epinephrine or formalin injection by depleting adrenal ascorbic acid levels 1 h after the stress (5, 24). The administration of ether, or laparotomy plus ether, on day 20 of gestation induce an immediate rise of fetal hypothalamic CRF and adrenal corticosterone (12, 27). All these results afford good evidence for an autonomous hypothalamic-hypophyseal-adrenocortical axis during the last days of gestation of the rat fetus. The purpose of the present report was to discover if the adrenal cortex was activated by the stress of labor and birth, as well as by adaptation of the newborn animal to new environmental conditions. The parameters examined were adrenal weight, the levels of adrenal ascorbic acid and corticosterone and the circulating corticosterone levels during the hours following birth.

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Section: Adrenal Weightsupporting

confidence: 91%

Section: Adrenal Corticosteronementioning

confidence: 90%

Increased Adrenocortical Activity in the Newborn Rat

Corbier¹,

Roffi²

1978

Neonatology

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“…These findings include increased fetal mortality, decreased fetal body and organ weights, cleft palate, altered placental morphology, delayed parturition, and added by this study, altered fetal adrenal corticosteroid production and ultrastructural development (Parvez et al, 1976;Ballard et al, 1977;Frank and Roberts, 1979;Garvey and Scott, 1981). The effects on the fetal adrenal glands appear to result from a direct inhibition of the hypothalamo-pituitary-adrenal axis by DEXA (D'Angelo et al, 1973;Dupouy and Coffigny, 1976). This interference with adrenotrophic influences is manifest in the present study by decreased adrenal weights and immature ultrastructural appearance of the cortical cells.…”

Section: Discussionmentioning

confidence: 57%

“…Fetal adrenal growth is also inhibited by high levels of circulating maternal corticosteroids which can cross the placenta and block fetal pituitary stimulation of the adrenals (Zarrow et al, 1970;D'Angelo et al, 1973;Milkovic and Domac, 1973;Klepac and Milkovic, 1979).…”

mentioning

confidence: 99%

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

et al. 1983

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The effects of maternal dexamethasone (DEXA) administration during the last days of gestation on fetal adrenal growth and differentiation were studied. Timed pregnant rats were divided into three groups: (a) 21d DEXA-3 received DEXA in drinking water (5 pg/ml) from days 18 to 21 of gestation; (b) 21d DEXAB received the same dosage of DEXA from days 15 to 21 of gestation; and (c) 21d control received tap water throughout gestation. On gestation day 21, pregnant rats were decapitated and bled into heparinized tubes; their fetuses were excised, weighed, decapitated, and bled. Fetal adrenals were prepared for electron microscopy or weighed and frozen until assayed for corticosterone. Control adrenals were also collected on day 15 of gestation and processed for electron microscopy only. Fetal adrenals were fixed in 2.5% glutaraldehyde in 0.5 M cacodylate buffer, postfixed in 2% osmium tetroxide (OsO$, dehydrated, and embedded in Epon 812. Twenty-one day (21d) fetal adrenal weights were 44% and 68% lower than control values for DEXA-3 and -6, respectively. Fetal adrenal corticosterone levels were decreased by 70% and 89% for the respective groups. These observations correlated with ultrastructural findings of decreased mitochondria1 number and size, altered orientation of the inner mitochondrial membrane, decreased lipid, and dilation of smooth endoplasmic reticulum (SER) in cortical fascicular cells of DEXA-exposed fetuses. Ultrastructural changes in the 21d DEXA fetal adrenals resembled 15d day control fetal adrenals. The results suggest suppressed adrenocortical differentiation probably due to DEXA inhibition of the steroidogenic influence of the fetal pituitary on the developing adrenal gland in DEXA-exposed fetuses.

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confidence: 99%

Influence of Cortisol on Trophic and Corticosteroidogenic Actions of Adrenocorticotrophin on Foetal Adrenals

Dupouy¹,

Herve²

1976

Journal of Endocrinology

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The treatment of female rats with corticosteroids during pregnancy, causes atrophy of the foetal adrenals (see Jost, 1966;Skebelskaya, 1968) and decreases the corticosterone content of the adrenals (D'Angelo, Paul & Wall, 1973). Corticosteroids are able to cross the placenta from the mother to the foetus. Adrenal atrophy also occurs when rat foetuses are injected with corticosteroids (see Jost, 1966). This effect is attributed to the blocking action of corticosteroids on the corticostimulating activity of the foetal hypophysis and not to the direct action of corticosteroids on the foetal adrenals. This hypothesis is supported by the atrophy of the foetal pituitary gland (see Jost, 1966) and by the decrease of its adrenocorticotrophin (ACTH) content (Skebelskaya, 1968) when mothers or foetuses are treated with corticosteroids. Moreover, foetal adrenal weight increases when foetuses are injected with cortisol and ACTH (Jost, 1957). Corticosteroids also prevent the adrenal hypertrophy observed after the treatment of the mother with inhibitors of steroidogenesis (Dupouy, 1971).The aim of this work was to verify whether corticosteroids could interfere directly with the trophic and corticosteroidogenic actions of ACTH at the level of the foetal adrenals. Both effects of ACTH were compared in decapitated rat foetuses, with and without cortisol administration.Twenty-one-day-old rat foetuses of the Wistar strain, were decapitated in utero, under pentobarbitone anaesthesia, and injected s.c. 30 min later with either l-6mu. porcine ACTH in 0-9% saline or with the same volume of saline only. Some foetuses were previously injected with cortisol acetate (600 µg) either just at the moment of decapitation or 30 min after this operation just at the time of the ACTH injection. Corticosterone determinations in the adrenals were made by the fluorometric method of Guillemin, Clayton, Lipscomb & Smith (1959).The corticosterone contents of the adrenals of the decapitated and non-cortisol-treated foetuses, increased lOmin after ACTH injection (Fig. 1). This response to ACTH was not impaired by cortisol treatment for 10 or 40 min (Fig. 1). The body and adrenal weights of the foetuses were not altered by the operation.Other foetuses were decapitated on day 20 of pregnancy and injected with 0-9% NaCl solution or with cortisol (600Mg). On day 21, the adrenals of the saline-treated foetuses were as atrophied (l-96±0-09 (s.EM.)mg, 8 cases) as those of the cortisol-treated foetuses (1-80 ±0-08 mg, 14 cases) when compared with the adrenals of the foetuses of the same age, decapitated on day 21 and injected with saline (2-44±0-10mg, 12 cases) or cortisol (2-51 ±0-11 mg,7 cases). Moreover, their adrenals contained little corticosterone (Fig. 1). The response of the decapitated foetuses to ACTH treatment was not affected by previous

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Maternal-fetal endocrine interrelations: influence of maternal adrenocorticosteroids on fetal ACTH secretion

Cited by 18 publications

References 0 publications

Increased Adrenocortical Activity in the Newborn Rat

Increased Adrenocortical Activity in the Newborn Rat

Suppression of adernal cortical growth and differentiation in fetal rats exposed to dexamethasone

Influence of Cortisol on Trophic and Corticosteroidogenic Actions of Adrenocorticotrophin on Foetal Adrenals

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