title: Analysis of hyposmolarity-induced taurine efflux pathways in the bullfrog sympathetic ganglia.
abstract: Hyposmolarity-induced taurine release was dependent on the decrease in medium osmolarity (5-50%) in the satellite glial cells of the bullfrog sympathetic ganglia. Release of GABA induced by hyposmolarity was much less than that of taurine. Omission of external Cl- replaced with gluconate totally suppressed taurine release, but only slightly suppressed GABA release. Bumetanide and furosemide, blockers of the Na+/K+/2Cl- cotransport system, inhibited taurine release by about 40%. Removal of external Na+ by replacement with choline, or omission of K+, suppressed taurine release by 40%. Antagonists of the Cl-/HCO3 exchange system, SITS, DIDS and niflumic acid, significantly reduced taurine release. The carbonic anhydrase inhibitor, acetazolamide, reduced the taurine release by 34%. Omission of external HCO3 by replacement with HEPES caused a 40% increase in the hyposmolarity-induced taurine release. Hyposmolarity-induced GABA release was not affected by bumetanide or SITS. Chloride channel blockers, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and N-phenylanthranilic acid (DPC), practically abolished taurine release. Blockers of K+ channels, clofilium and quinidine, had no effect on the taurine release. The hyposmolarity-induced taurine release was considerably enhanced by a simultaneous increase in external K+. GABA was not mediated by the same transport pathway as that of taurine. These results indicate that Cl- channels may be responsible for the hyposmolarity-induced taurine release, and that Na+/K+/2Cl- cotransporter and Cl-/HCO3 exchanger may contribute to maintain the intracellular Cl- levels higher than those predicted for a passive thermodynamic distribution in the hyposmolarity-induced taurine release.
authors.affiliation: Department of Physiology, Tokyo Medical University, Japan. s-sakai@tokyo-med.ac.jp
authors.forename: S
authors.initials: S
authors.lastname: Sakai
authors.forename: T
authors.initials: T
authors.lastname: Tosaka
mesh_terms: D000818:Animals; D017920:Antiporters / Q000378:metabolism; D001692:Biological Transport; D002352:Carrier Proteins / Q000378:metabolism; D018118:Chloride Channels / Q000378:metabolism; D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides / Q000378:metabolism; D005728:Ganglia, Sympathetic / Q000378:metabolism*; D009994:Osmolar Concentration; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000378:metabolism; D011892:Rana catesbeiana; D028021:Sodium-Potassium-Chloride Symporters; D013654:Taurine / Q000378:metabolism*; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D017920:Antiporters; D002352:Carrier Proteins; D018118:Chloride Channels; D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides; D015221:Potassium Channels; D028021:Sodium-Potassium-Chloride Symporters; D013654:Taurine; D005680:gamma-Aminobutyric Acid; D011188:Potassium