title: Amino acid efflux and cell volume regulation in cerebrocortical minislices prepared from chronically hyponatraemic and hypernatraemic rats.
abstract: The rates of efflux of pre-loaded amino acids, and associated steady-state volumes, were measured in cells in cerebrocortical minislices prepared from chronically (4 day) hypo- and hypernatraemic rats. The findings were compared with those obtained when cells from normonatraemic rats were acutely exposed to comparable levels of anisosmotic stress. In the presence of 122 mmol/l Na+ cells from normal rats showed increases in the rates of efflux of D-aspartate and GABA, and significant swelling (both by comparison with levels in media containing 142 mmol/l Na+). Conversely there was no acceleration of efflux in cells from hyponatraemic rats (plasma Na+ = 119-126 mmol/l) and volumes were preserved at levels comparable with those in isomotically incubated cells from normal rats. In media containing 164 mmol/l Na+ amino acid efflux in cells from normal rats was retarded, and shrinkage occurred. In cells from chronically hypernatraemic rats (plasma Na+ = 160-166 mmol/l) the rates of efflux of D-aspartate and D-glutamate were accelerated by comparison with cells from normal rats, with volume preservation. However there was no increase in the rate of GABA or glycine efflux, and cell swelling was observed. It is concluded (i) that during chronic hyponatraemia the presence of D-aspartate or GABA is associated with cell volume preservation, (ii) during chronic hypernatraemia acidic, but not neutral, amino acids are also effective in this respect, and (iii) that the markedly differing patterns of efflux responses to acute and chronic anisosmotic stress are likely to reflect chronic volume-regulatory adaptations of the efflux mechanism(s).
authors.affiliation: Department of Cell Physiology and Pharmacology, University of Leicester, UK. rol1@le.ac.uk
authors.forename: R O
authors.initials: RO
authors.lastname: Law
mesh_terms: D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid / Q000494:pharmacology; D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001224:Aspartic Acid / Q000378:metabolism; D001692:Biological Transport / Q000187:drug effects; D048429:Cell Size; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D002908:Chronic Disease; D005033:Ethylmaleimide / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism; D006955:Hypernatremia / Q000378:metabolism* / Q000473:pathology; D007010:Hyponatremia / Q000378:metabolism* / Q000473:pathology; D008297:Male; D009997:Osmotic Pressure; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000494:pharmacology; D014268:Trifluoperazine / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000596:Amino Acids; D014268:Trifluoperazine; D001224:Aspartic Acid; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid; D012964:Sodium; D005033:Ethylmaleimide; D017878:4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid