TAURINE EFFLUX AND CELL-VOLUME REGULATION IN CEREBRAL CORTICAL SLICES DURING CHRONIC HYPERNATREMIA

Efflux of cellular taurine from pre-loaded cerebral cortical slices incubated in hypo- and hyperosmotic media has been studied in normal and chronically hypernatraemic rats. Significant differences in transport mechanisms between the two groups has been noted. Hyperosmotic media retard efflux in cells from normal animals, with associated cell shrinkage, but accelerate efflux in cells from hypernatraemic rats, in which cell volumes are well maintained at pre-hypernatraemic levels. In hypernatraemic rats an anionic component of taurine efflux, present in normal animals, is lacking. Conversely, a distinct, calmodulin-dependent component which in normal rats is stimulated only in hypo-osmotic media, is present in both hypo- and hyperosmotically incubated slices from hypernatraemic rats, and inhibition of calmodulin-activation leads to cell swelling. This altered pattern of efflux and cell volume-regulation persists for at least 5 h following recovery from hypernatraemia, but remits by 30 h, indicating slow down-regulation of the hypernatraemically activated calmodulin-dependent efflux pathway and re-expression of anionic taurine transport.