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Mitochondrial development is impaired in hyperoxic rats and this may underpin the blunting of the acute hypoxic ventilatory response
Author(s) -
Fayyad Tariq H,
Rakoczy Ryan J,
Hartpence Annah J,
Wyatt Christopher N
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.1072.4
Subject(s) - carotid body , hyperoxia , hypoxia (environmental) , hypoxic ventilatory response , mitochondrial ros , mitochondrion , medicine , endocrinology , biology , chemistry , microbiology and biotechnology , oxygen , electrophysiology , respiratory system , lung , organic chemistry
Carotid body (CB) responses to hypoxia are low at birth and increase over time to mature responses. Using an in vitro rat CB‐carotid sinus nerve (CSN) preparation, Kholwadwala and Donnelly (1992) demonstrated that the CSN activity in response to hypoxia increased from low levels to robust adult responses after two weeks. This time course of maturation was paralleled by an increase in TASK channel sensitivity to hypoxia in the O 2 ‐sensing Type I cells (Kim et al , 2011). Previous studies have indicated that a fall in Type I cell mitochondrial volume and an increase in the rate of oxidative phosphorylation may underpin the development of the hypoxic ventilatory response (Paulet et al , 2012). Our most recent studies addressed the phenomenon that hyperoxia delays the maturation of the acute hypoxic response (Bavis, RW et al , 2010). Our initial findings suggest that hyperoxia caused the juvenile non‐oxygen‐sensing Type I cells to remain locked in a mitochondrial rich state and that as the rat developed this mitochondrial rich state impaired development of the hypoxic response. Thus there appears to be a correlation between mitochondrial volume and the ability to respond to hypoxia in rat Type I cells. Support or Funding Information NIH RO1 HL091836