Hydrogen Sulfide and Hypoxia‐Induced Changes in K2P3/9 (TASK) current and [Ca2+]i in Rat Carotid Body Glomus Cells

Abstract

Acute hypoxia depolarizes carotid body chemoreceptor (glomus) cells and elevates intracellular Ca2+ concentration ([Ca2+]i). Recent studies suggest that hydrogen sulfide (H2S) may serve as an oxygen sensor/signal in the carotid body during acute hypoxia. To further test such a role for H2S, we studied the effects of NaHS (a H2S 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 H2S, 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 H2S 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 H2S does not mediate the hypoxia‐induced changes in TASK activity and [Ca2+]i in rat glomus cells.