Literature DB >> 3280659

Adrenomedullary catecholamine release in the fetus and newborn: secretory mechanisms and their role in stress and survival.

T A Slotkin1, F J Seidler.   

Abstract

Catecholamines released by the adrenal medulla during birth play a key role in the adaptation of the newborn to extrauterine life. Respiratory, metabolic and cardiovascular adaptations to the hypoxia and other stresses associated with delivery are dependent upon a profound surge of adrenomedullary activity which occurs despite the immaturity of connections between the central nervous system and the adrenal. The "non-neurogenic" response seen in the fetus and neonate is thus essential to survival, and any interference either with catecholamine release or with catecholamine actions at adrenergic targets results in loss of the ability to survive hypoxia or other stressors. The immature secretory mechanism disappears as a result of development of neural connections, and factors which accelerate ontogeny of neural competence thus lead to premature loss of non-neurogenic secretory capabilities and a consequent increase in vulnerability. The fetus and neonate also have unusual proportions of adrenergic receptor subtypes in many tissues; these confer reactivity to specific stimuli associated with birth and with periods in which tissue differentiation may be under adrenergic control. Again, the ontogenetic switchover of receptor-mediated mechanisms appears to be a function of the development of neuronal competence, but in this case an important role may be played by a secondary surge in sympathetic tone occurring during the postnatal period. Through specialized mechanisms mediating catecholamine secretion and adrenergic responses, the adrenal medulla thus appears to provide both physiological and trophic signals to the fetus and neonate.

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Year:  1988        PMID: 3280659

Source DB:  PubMed          Journal:  J Dev Physiol        ISSN: 0141-9846


  26 in total

1.  Morphometric analyses of adrenal gland growth in fetal and neonatal sheep. II. The adrenal medulla, with some observations on its ultrastructure.

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2.  Developmental loss of hypoxic chemosensitivity in rat adrenomedullary chromaffin cells.

Authors:  R J Thompson; A Jackson; C A Nurse
Journal:  J Physiol       Date:  1997-01-15       Impact factor: 5.182

Review 3.  Adenosine A₂a receptors and O₂ sensing in development.

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4.  Oxygen-sensing mechanisms are present in the chromaffin cells of the sheep adrenal medulla before birth.

Authors:  G Y Rychkov; M B Adams; I C McMillen; M L Roberts
Journal:  J Physiol       Date:  1998-06-15       Impact factor: 5.182

5.  Regulation of Ca2+ signaling by acute hypoxia and acidosis in rat neonatal cardiomyocytes.

Authors:  José-Carlos Fernández-Morales; Martin Morad
Journal:  J Mol Cell Cardiol       Date:  2017-10-12       Impact factor: 5.000

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Review 7.  Infant bonding and attachment to the caregiver: insights from basic and clinical science.

Authors:  Regina Sullivan; Rosemarie Perry; Aliza Sloan; Karine Kleinhaus; Nina Burtchen
Journal:  Clin Perinatol       Date:  2011-10-19       Impact factor: 3.430

Review 8.  Revisiting the stimulus-secretion coupling in the adrenal medulla: role of gap junction-mediated intercellular communication.

Authors:  Claude Colomer; Michel G Desarménien; Nathalie C Guérineau
Journal:  Mol Neurobiol       Date:  2009-05-16       Impact factor: 5.590

9.  Chronic nicotine blunts hypoxic sensitivity in perinatal rat adrenal chromaffin cells via upregulation of KATP channels: role of alpha7 nicotinic acetylcholine receptor and hypoxia-inducible factor-2alpha.

Authors:  Josef Buttigieg; Stephen Brown; Alison C Holloway; Colin A Nurse
Journal:  J Neurosci       Date:  2009-06-03       Impact factor: 6.167

10.  Glucocorticoid feedback control of corticotropin in the hypoxic neonatal rat.

Authors:  Hershel Raff; Lauren Jacobson
Journal:  J Endocrinol       Date:  2007-02       Impact factor: 4.286

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