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Hypoxia-regulated catecholamine secretion in chromaffin cells.

Colin A Nurse1, Shaima Salman2, Angela L Scott3

  • 1Department of Biology and Molecular Medicine, McMaster University, 1280 Main St. West, Hamilton, ON, L8S 4K1, Canada. nursec@mcmaster.ca.

Cell and Tissue Research
|October 21, 2017
PubMed
Summary

Neonatal adrenal chromaffin cells (AMC) secrete catecholamines (CAT) in response to hypoxia via a non-neurogenic pathway. This crucial adaptation for extra-uterine life is lost postnatally but can be re-acquired by denervated adult AMC.

Keywords:
Adrenal medullaHypoxia inducible factor (HIF)-2αK+ channelsMitochondriaT-type calcium channels

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Area of Science:

  • Physiology
  • Neuroendocrinology
  • Developmental Biology

Background:

  • Adrenal catecholamine (CAT) secretion is a key physiological response to hypoxia, vital for homeostasis and organ protection.
  • In adult mammals, CAT secretion is primarily mediated by sympathetic nervous system activation of adrenomedullary chromaffin cells (AMC) via the splanchnic nerve.
  • Neonatal mammals exhibit hypoxia-induced, non-neurogenic CAT secretion due to immature or absent splanchnic innervation, critical for adapting to extra-uterine life.

Purpose of the Study:

  • To review current understanding of direct acute hypoxia sensing mechanisms in perinatal AMC.
  • To explore how postnatal development and splanchnic innervation regulate CAT secretion.
  • To discuss plasticity mechanisms involved in CAT secretion during chronic and intermittent hypoxia.

Main Methods:

  • This review synthesizes existing research on hypoxia sensing and CAT secretion in AMC.
  • Focuses on perinatal physiology and postnatal developmental regulation.
  • Includes discussion of denervation studies and plasticity mechanisms.

Main Results:

  • Neonatal AMC possess a direct hypoxia-sensing mechanism for CAT secretion, independent of neural input.
  • This non-neurogenic pathway is gradually suppressed postnatally with the maturation of splanchnic innervation.
  • Adult AMC can re-acquire direct hypoxia-sensing capabilities upon denervation, indicating plasticity.

Conclusions:

  • The perinatal non-neurogenic hypoxia-sensing pathway in AMC is essential for neonatal adaptation.
  • Postnatal development and innervation dynamically regulate this mechanism.
  • Plasticity in AMC allows for the re-emergence of hypoxia sensitivity in adult states, offering insights into physiological adaptation.