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Regulation of Oxygen Sensitivity in Adrenal Chromaffin Cells
Author(s) -
Nurse Colin A.,
Buttigieg Josef,
Brown Stephen,
Holloway Alison C.
Publication year - 2009
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2009.05031.x
Subject(s) - chromaffin cell , nicotinic agonist , endocrinology , nicotine , medicine , cholinergic , stimulation , depolarization , chemistry , hypoxia (environmental) , acetylcholine receptor , catecholamine , downregulation and upregulation , receptor , adrenal medulla , biology , oxygen , biochemistry , organic chemistry , gene
Adrenomedullary chromaffin cells (AMC) possess a direct hypoxia‐sensing mechanism that promotes a vital catecholamine surge at birth. This mitochondria‐dependent adaptive mechanism is suppressed postnatally as AMC acquire cholinergic innervation, and it is mediated by K + channel inhibition, membrane depolarization, and voltage‐gated Ca 2+ entry. We hypothesized that nicotinic ACh receptor (AChR) activation might contribute to this postnatal loss of O 2 sensitivity. Following in utero nicotinic AChR activation, via maternal administration of nicotine bitartrate, hypoxic sensitivity was suppressed in neonatal AMC. Similarly, when neonatal AMC or immortalized chromaffin (MAH) cells were cultured for ∼7 d with nicotine base (50 μM), hypoxic sensitivity was suppressed. This effect required α7 nAChR stimulation, and involved upregulation of K ATP channels, which are activated during hypoxia. Thus, nicotinic AChR activation may contribute to the suppression of hypoxic sensitivity in AMC, and this pathway could provide the basis for the loss of hypoxia tolerance in the offspring of smoking mothers.