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PubMed · 165838

Effect of decapitation and ACTH on somatic development of the rabbit fetus.

P M Jack·R D Milner
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Abstract

Rabbit fetuses were decapitated, injected with ACTH or decapitated and injected with ACTH on day 24 of gestation. On day 29 the body weight and weight of the interscapular fat pad were compared with those of littermates. The weight, total DNA and weight/DNA ratio of the liver, heart and kidney were measured in experimental and control fetuses. A comparison was made between decapitated and control fetuses of the length of the hind limb bones and number of ossified vertebrae. The body weight of the decapitated or ACTH-injected fetus ranked significantly below the mean for the litter, but decapitated fetuses injected with ACTH ranked close to the litter mean. The growth retardation of the decapitated fetus was not manifest in the kidneys which were heavier and had a greater number of cells than normal, nor in the cell size of the heart, liver or kidneys which were equal to those of the heaviest fetus in the litter. Decapitation had no specific effect on ossification. Growth retardation of the ACTH-injected fetus was mirrored by different patterns of DNA and weight/DNA reduction in the three organs studied. Decapitation retards growth in body weight of the fetal rabbit which may be corrected by ACTH. It is concluded that the hypophyseal-adrenal axis plays a role in the control of normal fetal growth but that excess secretion of glucocorticoids results in stunting.

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Adrenocorticotropic HormoneAnimalsBody WeightDNAFemaleFetusHeadHeartKidneyLiverMyocardiumOrgan SizePregnancyRabbitsComparative StudyJournal Article

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BibTeXRIS

P M Jack, R D Milner. 1975. Effect of decapitation and ACTH on somatic development of the rabbit fetus.. https://doi.org/10.1159/000240730

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PubMed1979

[Factor(s) controlling the secretion of adrenocorticotropin (ACTH) in peripheral plasma (author's transl)].

The factor(s) controlling the secretion of ACTH in peripheral plasma are not well known. The effects of non-extracted and extracted plasma on ACTH secretion were investigated using rat anterior pituitary cell cultures. Medium ACTH was assayed by radioimmunoassay, and the corticotropin releasing activity (CRA) was expressed as ACTH released. One hundred ul of non-extracted plasma showed significant CRA, whereas greater volumes of plasma showed reduced activity. Non-extracted plasma (250 approximately 500 microliter) rather reduced the secretion of ACTH evoked by hypothalamic extract (HE). When plasma was extracted with 0.2 N-acetic acid-acetone and divided into an acid phase and an acetone-ether phase by adding ether, the CRA was recovered in the acid phase while no significant activity was observed in the acetone-ether phase. The acid phase extract of plasma showed a positive dose-response relationship between the amount of plasma extract (50 approximately 800 microliter plasma equivalent) and ACTH release in pituitary cell cultures. The organic phase of plasma extract inhibited HE-induced release of ACTH, and this ACTH-release inhibiting activity was presumed to be corticosterone. When the acid phase extract of 20 ml plasma was applied to a Sephadex G-25 (fine) and eluted with 0.2 N acetic acid, two peaks of CRA were observed. One eluted in the region of void volume and another eluted in the retarded region where no activity was found in chromatography of HE. HE increased both ACTH and cyclic AMP release, but the plasma extract reduced cyclic AMP release. These results suggest that plasma contains both CRA and ACTH release inhibiting activity which can be extracted separately, and that plasma CRA is different from the hypothalamic corticotropin releasing factor.

Adrenocorticotropic Hormone↗