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Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

Departamento de Bioquímica y Biología Molecular y Fisiología. Facultad de Medicina. Universidad de Valladolid. Instituto de Biología y Genética Molecular-CSIC, 47005 Valladolid, Spain
Centro de Investigación Biomédica en Red de Enfermedades Respiratorias (CIBERES-ISCIII), 28029 Madrid, Spain
Division of Pulmonary, Allergy and Critical Care Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA
Department of Inflammation Biology, School of Immunology and Microbial Sciences, Faculty of Life Sciences and Medicine, King’s College, London SE1 1UL, UK
Author to whom correspondence should be addressed.
Antioxidants 2019, 8(3), 62;
Received: 12 December 2018 / Revised: 1 March 2019 / Accepted: 9 March 2019 / Published: 13 March 2019
(This article belongs to the Special Issue H2S in Redox Signaling)
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Carotid body (CB) chemoreceptor cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB chemoreceptor cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in cells. Based on its effects on the CB chemoreceptor cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels. View Full-Text
Keywords: carotid body; hydrogen sulfide; hypoxia; hydroxycobalamin; oxygen sensing carotid body; hydrogen sulfide; hypoxia; hydroxycobalamin; oxygen sensing

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).

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Gallego-Martin, T.; Prieto-Lloret, J.; Aaronson, P.I.; Rocher, A.; Obeso, A. Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells. Antioxidants 2019, 8, 62.

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