Absence of Transplacental Passage of ACTH in the Rat: Direct Experimental Proof

Abstract

In order to investigate whether ACTH can cross the placenta of the rat at term, porcine ¹²⁵I-ACTH was injected into mothers or fetuses. ACTHwas then extracted from maternal and fetal plasma, using QUSO G-32, 2.5, 5, 10, 15 and 20 min after the injection of labelled ACTH. Plasma samples were also chromatographed on Sephadex G-50, fine, columns, 5 and 20 min after the administration of ACTH. When ¹²⁵I-ACTH was injected into the mothers, the two methods used were unable to detect any radioactivity associated with intact ACTH in the fetal plasma. The same was observed in the maternal plasma when labelled hormone was administered to the fetuses. These observations provide direct experimental proof of the absence of transplacental passage in the rat of ¹²⁵I-ACTH from the mother to the fetus as well as from the fetus to the mother.

Developmental Changes in Fetal Adrenal Hypertrophy following Maternal Bilateral and Fetal Unilateral Adrenalectomy at Different Stages of Gestation in the Rat

“…Also, there are some lines of evidence that the hypothalamus begins to control the pituitary-adrenal system before birth [5,10,11,16], though evidence indi cates that the onset of the hypothalamic con trol occurs slightly later than that of the pitu itary regulation of the adrenal [9], Adrenalectomy of pregnant rats results in a hypertrophy of the fetal adrenals near the end of gestation and just after birth [21], a phenomenon which is considered a compen satory event in the fetus owing to maternal adrenocortical deficiency. In relation to this, it will be pertinent to mention that maternal ACTH cannot cross the placenta [7], but cor ticoids can [1,6], Thus, the compensatory hypertrophy of fetal adrenals after maternal adrenalectomy is interpreted as a result of the negative feedback response of the fetal pitu itary-adrenal system to the declined amount of fetal circulating corticoids derived from the mother. Fetal unilateral adrenalectomy causes a significant hypertrophy of the fetal contralateral adrenal at the end of gestation as well [8], a phenomenon which is also con sidered a result of the fetal pituitary-adrenal feedback response.…”

Immunohistochemical localization of the ACTH (MC-2) receptor in the rat placenta and adrenal gland

“…Furthermore, direct experimental evidence indicates the lack of a transplacental passage of 125 I-ACTH from the pregnant rat to the fetus as well as from the fetus to the mother (Dupouy et al, 1980). In the human placenta, the expression of corticotropin-releasing factor (CRF) increases as much as 100 times during the last 6 to 8 weeks of pregnancy and is paradoxically stimulated by glucocorticoids (Majzoub and Karalis, 1999).…”

Maternal Adrenalectomy Abrogates the Effect of Fetal Alcohol Exposure on the Interleukin-1β-Induced Febrile Response: Gender Differences

“…Previous research demonstrated that alcohol consumption increases plasma corticosterone levels in the dams [7, 22], and that this glucocorticoid can cross the placenta and influence the development of the fetal HPA axis [23]. Furthermore, maternal ADX has been shown to prevent various effects of FAE on the HPA axis.…”