Journal article
Chronic Nicotine Blunts Hypoxic Sensitivity in Perinatal Rat Adrenal Chromaffin Cells via Upregulation of KATP Channels: Role of α7 Nicotinic Acetylcholine Receptor and Hypoxia-Inducible Factor-2α
Abstract
Fetal nicotine exposure blunts hypoxia-induced catecholamine secretion from neonatal adrenomedullary chromaffin cells (AMCs), providing a link between maternal smoking, abnormal arousal responses, and risk of sudden infant death syndrome. Here, we show that the mechanism is attributable to upregulation of K(ATP) channels via stimulation of alpha7 nicotinic ACh receptors (AChRs). These K(ATP) channels open during hypoxia, thereby suppressing …
Authors
Buttigieg J; Brown S; Holloway AC; Nurse CA
Journal
Journal of Neuroscience, Vol. 29, No. 22, pp. 7137–7147
Publisher
Society for Neuroscience
Publication Date
June 3, 2009
DOI
10.1523/jneurosci.0544-09.2009
ISSN
0270-6474
Associated Experts
Fields of Research (FoR)
Sustainable Development Goals (SDG)
Medical Subject Headings (MeSH)
Adrenal GlandsAnalysis of VarianceAnimalsAnimals, NewbornBasic Helix-Loop-Helix Transcription FactorsCadmiumCalciumCalcium Channel BlockersCatecholaminesCell HypoxiaCells, CulturedChromaffin CellsDrug InteractionsElectrochemistryEnzyme InhibitorsFemaleGlyburideMembrane PotentialsNicotineNicotinic AgonistsPatch-Clamp TechniquesPeptidesPotassium Channels, Inwardly RectifyingPregnancyProtein Kinase CRatsRats, WistarReceptors, NicotinicUp-Regulationalpha7 Nicotinic Acetylcholine Receptor