Volume‐sensitive release of taurine from cultured astrocytes: Properties and mechanism

Release of taurine in response to cell swelling induced by hyposmolarity was observed in cultured astrocytes. Efflux of 3 H‐taurine increased by 30% and 70% upon reductions in osmolarity of only 5% and 10%. Reductions in osmolarity of 20%, 30%, and 50% stimulated basal taurine release by 300%, 500%, and 1,500%, respectively. The properties of this volume‐sensitive release of taurine were examined to investigate: 1) its association with K + and Cl − fluxes, currently activated during volume regulation; 2) its relationship with Ca 2+ ‐dependent reactions; and 3) the mechanism of the taurine efflux process. Taurine release was unaffected by removal of Na + , Ca 2+ , or Cl − , by pimozide and trifluoperazine, or by agents disrupting the cytoskeleton. The K + channel inhibitors barium, quinidine, tetraethylammonium, and gadolinium had no effect. Taurine release was reduced by furosemide, a blocker of K + /Cl − cotransport, but not by the more specific inhibitor, bumetanide. It was markedly reduced by the inhibitors of Cl − channels DIDS, SITS, and anthracene‐9‐carboxylate. Taurine efflux was pH‐dependent, being reduced at low pH values. It was decreased at 4°C but not at 14°C or 20°C. These results suggest that the volume‐sensitive release of taurine is independent of K + fluxes but may be associated with Cl − conductances. It also seems unrelated to Ca 2+ ‐dependent transduction mechanisms. The Na + ‐dependent taurine carrier apparently is not involved in the swelling‐induced release process.