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Hydrogen Sulfide and Hypoxia‐Induced Changes in K2P3/9 (TASK) current and [Ca 2+ ] i in Rat Carotid Body Glomus Cells
Author(s) -
Kim Donghee,
Wang Jiaju,
Kim Insook,
Carroll John
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.682.8
Subject(s) - carotid body , hypoxia (environmental) , glomus cell , cystathionine beta synthase , chemistry , intracellular , hydrogen sulfide , aminooxyacetic acid , endocrinology , medicine , biophysics , biochemistry , chemoreceptor , oxygen , cysteine , biology , enzyme , sulfur , receptor , organic chemistry , stimulation
Acute hypoxia depolarizes carotid body chemoreceptor (glomus) cells and elevates intracellular Ca 2+ concentration ([Ca2+]i). Recent studies suggest that hydrogen sulfide (H 2 S) may serve as an oxygen sensor/signal in the carotid body during acute hypoxia. To further test such a role for H 2 S, we studied the effects of NaHS (a H 2 S donor) on the activity of TASK channel and intracellular [Ca2+]i, which are considered crucial for mediating the hypoxic response. Like hypoxia, NaHS inhibited TASK activity and elevated [Ca2+]i. To block the production of H 2 S, glomus cells were incubated (3 hr) with DL‐propargylglycine, aminooxyacetic acid, beta‐cyano‐L‐alanine (0.3 mM) that inhibit cystathionine‐beta‐synthase and cystathionine‐gamma‐lyase. Cell H 2 S production induced by L‐cysteine and hypoxia was strongly reduced by the inhibitors, as assessed using SF‐7 fluorescence. In cells treated with inhibitors, the hypoxia‐induced reduction of TASK activity and elevation of [Ca2+]i were similar in magnitude to those observed in untreated cells. In control or inhibitor‐treated cells, BK channel was not open at rest. These findings suggest that H 2 S does not mediate the hypoxia‐induced changes in TASK activity and [Ca2+]i in rat glomus cells.