The Effect of Hypophysial Hormones and Human Chorionic Gonadotrophin (Hcg) on the Anencephalic Fetal Adrenal Cortex and on Parturition in the Human

Honnebier, W. J.; Jöbsis, A. C.; Swaab, Dick F.

doi:10.1111/j.1471-0528.1974.tb00492.x

Cited by 48 publications

(12 citation statements)

References 62 publications

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“…In sheep, the fetal hypothalamic pituitary axis plays a key role in the onset of labor by triggering the release of corticotropin [38], whereas fetal oxytocin probably does not contribute to the mechanism underlying ovine parturition. Injection of posteriorlobe hormones into human anencephalic fetuses has produced maternal uterine contractions [34]. Oxytocin can cross the primate placenta in both directions without degradation, according to DAWOOD et al [16], However, to reach the myometrial receptor sites the hormone has to be circulated in the maternal bloodstream, and this pathway is likely to lead to its inactivation [39].…”

Section: Discussionmentioning

confidence: 99%

Plasma oxytocin in human pregnancy and parturition

Geest¹,

Thiéry²,

Piron-Possuyt³

et al. 1985

Journal of Perinatal Medicine

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Section: Discussionmentioning

confidence: 99%

Plasma oxytocin in human pregnancy and parturition

Geest¹,

Thiéry²,

Piron-Possuyt³

et al. 1985

Journal of Perinatal Medicine

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“…Morphologic studies of adrenal gland development from anencephalic and apituitary human fetuses have shown normal development prior to 15 weeks of gestation but subsequent atrophy of the inner fetal zone thereafter (10). Adrenal atrophy in human anencephalic fetuses was prevented by ACTH treatment in utero (11)(12)(13). These data strongly suggest that human fetal adrenal growth, and in particular the rapid growth of the fetal zone, is dependent upon an intact pituitary and may be regulated by ACTH.…”

Section: Introductionmentioning

confidence: 99%

Basic fibroblast growth factor expression is regulated by corticotropin in the human fetal adrenal: a model for adrenal growth regulation.

Mesiano

Mellon

Gospodarowicz

et al. 1991

Proc. Natl. Acad. Sci. U.S.A.

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Human fetal adrenal growth after midgestation is very rapid and appears to be dependent upon pituitary adrenocorticotropin (ACTH) in vivo. We hypothesized that the regulation of fetal adrenal growth by ACTH is mediated by ACTH-stimulated local growth factor production. As we have found basic fibroblast growth factor (bFGF) to be a potent mitogen for human fetal adrenal cells in culture, we conducted studies to determine whether bFGF is synthesized by the human fetal adrenal gland and whether bFGF gene expression in primary cultures of human fetal adrenal cells is regulated by ACTH. Bioassayable bFGF-like activity was detected in ex-

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“…It has been suggested that hCG stimulates the growth of the adrenal gland of the anencephalic fetus before 20 weeks gestation (20,41,55). However, Honnebier et al (58), who injected anencephalic fetuses with hCG before delivery, observed no demonstrable increase in steroid secretion. Recently, it has been reported that the adrenals of anencephalic abortuses are smaller and have reduced amounts of fetal zone cells by as early as 15 weeks gestation (83,105).…”

Section: Adrenal Tissue Of Human Anencephalic Abortuses and Newbmentioning

confidence: 96%

Lipoprotein Utilization and Cholesterol Synthesis by the Human Fetal Adrenal Gland*

Carr¹,

Simpson²

1981

Endocrine Reviews

145

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A model proposed for regulation of steroidogenesis, lipoprotein utilization and cholesterol metabolism in HFA tissue is presented in Fig 17. We envision that the role of ACTH and cAMP in steroidogenesis and cholesterol metabolism is as follows. ACTH binds to specific receptors on the surface of the cells of the HFA gland and as a consequence, adenylate cyclase is activated, leading to increased formation of cAMP. cAMP causes activation of protein kinase that leads, presumably, to phosphorylation of specific proteins. This leads to the initiation of reactions that give rise to increased activity of key enzymes and levels of proteins involved in adrenal cholesterol metabolism. Presumably, the action of ACTH causes an increase in the activity of cholesterol side chain cleavage, the rate-limiting step in the conversion of cholesterol to steroid hormones. We suggest that once the mitochondrial cholesterol side-chain cleavage system is fully activated by ACTH, the supply of cholesterol to the mitochondria becomes rate-limiting for steroidogenesis. To meet this demand for cholesterol, a further action of ACTH results in an increase in the number of LDL receptors. LDL binds to specific receptors on the cell surface that are localized in coated pits. LDL is internalized by a process of adsorptive endocytosis and the internalized vesicles fuse with lysosomes and the protein component of LDL is hydrolyzed by lysosomal proteolytic enzymes to amino acids. The cholesteryl esters of LDL also are hydrolyzed to give rise to fatty acids and cholesterol. The liberated cholesterol is available for utilization in the biosynthesis of steroid hormones and other cellular processes. In addition, ACTH stimulates the activity of HMG CoA reductase and, thus, the rate of de novo cholesterol biosynthesis. In this way sufficient cholesterol is obtained to provide for precursor cholesterol to maintain the high rate of steroid synthesis by the HFA. HDL is not utilized as a source of cholesterol by the HFA. Because of the rapid rate of utilization of LDL by the HFA, fetal plasma levels of LDL are low and the activity of the HFA is a primary determinant of these levels. Thus, in the case of anencephaly, in which the activity of the adrenal is very low, plasma levels of LDL are 2--3 times higher than in normal fetuses, whereas plasma HDL levels are similar. In addition, in the normal neonate plasma LDL levels rise rapidly after birth, and this event is coincident with the involution of the fetal zone of the adrenal. The fetal liver is likely to be the major source ultimately of the LDL-cholesterol utilized by the HFA. Consequently, factors that regulate cholesterol and lipoprotein synthesis in the fetal liver may, in turn, affect the steroidogenic activity of the HFA through regulation of the supply of cholesterol precursor. Thus, if trophic factors for the HFA other than ACTH exist, an important site of their action might be the fetal liver, rather than a direct action to influence the rate of synthesis of steroids by the fetal adrenal.

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The Effect of Hypophysial Hormones and Human Chorionic Gonadotrophin (Hcg) on the Anencephalic Fetal Adrenal Cortex and on Parturition in the Human

Cited by 48 publications

References 62 publications

Plasma oxytocin in human pregnancy and parturition

Plasma oxytocin in human pregnancy and parturition

Basic fibroblast growth factor expression is regulated by corticotropin in the human fetal adrenal: a model for adrenal growth regulation.

Lipoprotein Utilization and Cholesterol Synthesis by the Human Fetal Adrenal Gland*

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