Cells in slices prepared from the superficial cerebral cortex of normonatra
emic rats underwent moderate swelling when exposed to low Na+ medium (122 m
mol/l) accompanied by a large increase in the rate of efflux of preloaded t
aurine. In contrast, cells in slices from chronically (4 day) hyponatraemic
rats did not increase in volume and the rate of taurine efflux was unchang
ed. The anion transport inhibitor 4,4'-diisothiocyanato-stilbene-2,2'-sulph
onic acid (25 mu mol/l) caused marked (-44%) reduction in taurine efflux in
cells from normonatraemic rats; this response was strongly attenuated (-16
%) by hyponatraemia. When slices from hyponatraemic rats were acutely expos
ed to medium containing 142 mmol/Na+ cells exhibited marked and paradoxical
swelling. This response was completely abolished by the NaCl co-transport
inhibitor bumetanide (50 mu mol/l) and was not observed in slices that had
not been pre-loaded with taurine. Forty eight hours after the start of the
remission of hyponatraemia, cells from post-hyponatraemic rats displayed no
rmal responses (i.e., moderate swelling and greatly accelerated taurine eff
lux) on exposure to 122 mmol/Na+. But at 24 h there was only partial restor
ation of the efflux response to 122 mmol/Na+, with an enhanced cell swellin
g response that was not significantly affected by bumetanide. II is conclud
ed that (i) during chronic hyponatraemia, unlike acute hyposmotic stress, c
ortical cells preserve their volume and that this is not associated with an
y increase in the rate of taurine loss; there does however, appear to be a
decrease in the anionic component of cellular taurine efflux; (ii) acute re
-incubation of slices in medium containing 142 mmol/l Na+ is associated wit
h cell swelling that may reflect up-regulation of Na/Cl/taurine co-transpor
t; (iii) following restoration of normonatraemia the pattern of normal cell
ular response to acute hyposmotic stress is only gradually re-established.
(C) 1998 Elsevier Science Ltd. All rights reserved.