Abstract
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 Ca2+ entry. We hypothesized that nicotinic ACh receptor (AChR) activation might contribute to this postnatal loss of O2 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 approximately 7 d with nicotine base (50 muM), hypoxic sensitivity was suppressed. This effect required alpha7 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.
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