RT info:eu-repo/semantics/article
T1 Hydroxycobalamin reveals the involvement of hydrogen sulfide in the hypoxic responses of rat carotid body chemoreceptor cells
A1 Gallego Martín, Teresa
A1 Prieto Lloret, Jesús
A1 Aaronson, Philip Irving
A1 Rocher Martín, María Asunción
A1 Obeso Cáceres, Ana María de la Luz
K1 Carotid body
K1 Cuerpo carotídeo
K1 Hydrogen sulfide
K1 Ácido sulfhídrico
K1 Hypoxia
K1 Hipoxia
K1 Hydroxycobalamin
K1 Hidroxocobalamina
AB 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.
PB MDPI
SN 2076-3921
YR 2019
FD 2019
LK https://uvadoc.uva.es/handle/10324/56465
UL https://uvadoc.uva.es/handle/10324/56465
LA eng
NO Antioxidants, 2019, vol. 8, n. 3, 62
NO Producción Científica
DS UVaDOC
RD 23-nov-2024