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Lookup NU author(s): Dr Seva TelezhkinORCiD
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Recent evidence suggests that H(2)S contributes to activation of the carotid body by hypoxia by inhibiting K(+) channels. Here, we determine both the molecular identity of the K(+) channel target within the carotid body and the biophysical characteristics of the H(2)S-evoked inhibition by analyzing native rat and human recombinant BK(Ca) channel activity in voltage-clamped, inside-out membrane patches. Rat glomus cells express the enzymes necessary for the endogenous generation of H(2)S, cystathionine-beta-synthase and cystathionine-gamma-lyase. H(2)S inhibits native carotid body and human recombinant BK(Ca) channels with IC(50) values of around 275 microM. Inhibition by H(2)S is rapid and reversible, works by a mechanism which is distinct from that suggested for CO gas regulation of this channel and does not involve an interaction with either the "Ca bowl" or residues distal to this Ca(2+)-sensing domain. These data show that BK(Ca) is a K(+) channel target of H(2)S, and suggest a mechanism to explain the H(2)S-dependent component of O(2) sensing in the carotid body.
Author(s): Telezhkin V, Brazier SP, Cayzac S, Wilkinson WJ, Riccardi D, Kemp PJ
Publication type: Article
Publication status: Published
Journal: Respiratory Physiology & Neurobiology
Year: 2010
Volume: 172
Issue: 3
Pages: 169-178
Print publication date: 31/07/2010
Online publication date: 16/05/2010
Acceptance date: 10/05/2010
ISSN (print): 1569-9048
ISSN (electronic): 1878-1519
Publisher: Elsevier BV
URL: https://doi.org/10.1016/j.resp.2010.05.016
DOI: 10.1016/j.resp.2010.05.016
PubMed id: 20576528
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