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Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
The carotid body oxygen sensor
Lin Gao1, Alejandro Moreno-Domínguez1, Patricia Ortega-Sáenz1
1Institute of Biomedicine of Seville (IBiS), University Hospital "Virgen del Rocío"/CSIC/University of Seville, Seville, Spain; Department of Medical Physiology and Biophysics. School of Medicine, University of Seville, Seville, Spain; CIBERNED, Madrid, Spain.
Abstract:
Carotid body (CB) chemoreceptor glomus cells sense hypoxia through the inhibition of plasmalemmal K+ channels, which leads to the opening of Ca2+ channels, Ca2+ influx, and neurotransmitter release. The mechanism of O2 sensing and the regulation of membrane ion channels by O2 have remained undefined and a subject of debate. Here, we summarize the molecular pathway that underlies acute O2 sensing in the CB. This process does not rely on a single-molecule O2 sensor expressed in glomus cells but rather on HIF2α-dependent genetically specialized mitochondria that can detect changes in O2 tension, within physiological ranges, and generate biochemical signals that regulate membrane ion channels. The acute O2-sensing pathway in glomus cells could provide new targets for respiratory and cardiovascular pharmacology.
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