CHOROID-PLEXUS POTASSIUM COTRANSPORT - MODULATION BY OSMOTIC-STRESS AND EXTERNAL POTASSIUM

Authors
Citation
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
Citations number
34
Categorie Soggetti
Biology,Neurosciences
Journal title
ISSN journal
00223042
Volume
64
Issue
6
Year of publication
1995
Pages
2747 - 2754
Database
ISI
SICI code
0022-3042(1995)64:6<2747:CPC-MB>2.0.ZU;2-1
Abstract
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.