Rf. Keep et Jm. Xiang, CHOROID-PLEXUS POTASSIUM COTRANSPORT - MODULATION BY OSMOTIC-STRESS AND EXTERNAL POTASSIUM, Journal of neurochemistry, 64(6), 1995, pp. 2747-2754
The choroid plexuses are involved in CSF secretion and CSF K homeostas
is. This study examines the potential role of K cotransport in these t
wo processes using isolated rat lateral ventricle choroid plexuses, Bu
metanide-sensitive Rb-86 influx and efflux were measured to assess the
response of K cotransport to changes in media osmolality and K concen
tration. Alterations in osmolality had no effect on K uptake (in the p
resence or absence of bumetanide). However, the efflux rate constant f
or K was 0.29 +/- 0.02, 0.44 +/- 0.04, and 0.84 +/- 0.06 min(-1) in 24
0, 300, and 424 mOsm/kg solutions, respectively (p < 0.001),This incre
ase in efflux with osmolality, an opposite effect to that found in man
y cells, was solely due to enhanced K cotransport. The increased cotra
nsport may be involved in limiting brain shrinkage during hyperosmotic
stress if the cotransporter is present on the apical membrane. The ra
te of bumetanide-sensitive efflux was unaffected by changes in externa
l [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-m
in exposure to 1 mM K. Sixty minutes of exposure to 1 mM [K] abolished
the bumetanide-sensitive K uptake present in plexuses exposed continu
ally to normal media. This modulation of K cotransport by external IK]
may be important in CSF K homeostasis by limiting K loss from the CSF
if CSF [K] is low.