tacrolimus and sodium-hydride

Acute hypoxia depolarizes carotid body chemoreceptor (glomus) cells and elevates intracellular Ca(2+) concentration ([Ca(2+)]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 H2S on the activity of TASK channel and [Ca(2+)]i, which are considered important for mediating the glomus cell response to hypoxia. Like hypoxia, NaHS (a H2S donor) inhibited TASK activity and elevated [Ca(2+)]i. To inhibit the production of H2S, glomus cells were incubated (3h) with inhibitors of cystathionine-β-synthase and cystathionine-γ-lyase (DL-propargylglycine, aminooxyacetic acid, β-cyano-L-alanine; 0.3 mM). SF7 fluorescence was used to assess the level of H2S production. The inhibitors blocked L-cysteine- and hypoxia-induced elevation of SF7 fluorescence intensity. In cells treated with the inhibitors, hypoxia produced an inhibition of TASK activity and a rise in [Ca(2+)]i, similar in magnitude to those observed in control cells. L-cysteine produced no effect on TASK activity or [Ca(2+)]i and did not affect hypoxia-induced inhibition of TASK and elevation of [Ca(2+)]i. These findings suggest that under normal conditions, H2S is not a major signal in hypoxia-induced modulation of TASK channels and [Ca(2+)]i in isolated glomus cells.

Topics: Alkynes; Analysis of Variance; Animals; Animals, Newborn; Calcium; Carotid Body; Chemoreceptor Cells; Dose-Response Relationship, Drug; Gasotransmitters; Glycine; Hydrogen Sulfide; Hypoxia; Intracellular Fluid; Membrane Potentials; Nerve Tissue Proteins; Patch-Clamp Techniques; Potassium Channels, Tandem Pore Domain; Rats; Rats, Sprague-Dawley; Sodium Compounds; Tacrolimus; Time Factors