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Choroid Plexus Potassium Cotransport: Modulation by Osmotic Stress and External Potassium
Author(s) -
Keep Richard F.,
Xiang Jianming
Publication year - 1995
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1995.64062747.x
Subject(s) - bumetanide , cotransporter , chemistry , endocrinology , choroid plexus , medicine , efflux , osmotic concentration , homeostasis , potassium , biophysics , biochemistry , sodium , biology , central nervous system , organic chemistry
The choroid plexuses are involved in CSF secretion and CSF K homeostasis. This study examines the potential role of K cotransport in these two processes using isolated rat lateral ventricle choroid plexuses. Bumetanide‐sensitive 86 Rb influx and efflux were measured to assess the response of K cotransport to changes in media osmolality and K concentration. Alterations in osmolality had no effect on K uptake (in the presence or absence of bumetanide). However, the efflux rate constant for K was 0.29 ± 0.02, 0.44 ± 0.04, and 0.84 ± 0.06 min −1 in 240, 300, and 424 mOsm/kg solutions, respectively ( p < 0.001). This increase in efflux with osmolality, an opposite effect to that found in many cells, was solely due to enhanced K cotransport. The increased cotransport may be involved in limiting brain shrinkage during hyperosmotic stress if the cotransporter is present on the apical membrane. The rate of bumetanide‐sensitive efflux was unaffected by changes in external [K]. However, the rate of K uptake (measured on return to normal [K] media) was reduced gradually by exposure to low [K]. It was 21 ± 1, 19 ± 3, 13 ± 2, and 6 ± 1 nmol/mg/min after 0, 10, 30, and 60‐min exposure to 1 m M K. Sixty minutes of exposure to 1 m M [K] abolished the bumetanide‐sensitive K uptake present in plexuses exposed continually to normal media. This modulation of K cotransport by external [K] may be important in CSF K homeostasis by limiting K loss from the CSF if CSF [K] is low.