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Altered electrolyte handling of the choroid plexus in rats with glycerol‐induced acute renal failure
Author(s) -
Ishikawa Atsuko,
Kono Kentaro,
Sakae Rie,
Aiba Tetsuya,
Kawasaki Hiromu,
Kurosaki Yuji
Publication year - 2010
Publication title -
biopharmaceutics and drug disposition
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.419
H-Index - 58
eISSN - 1099-081X
pISSN - 0142-2782
DOI - 10.1002/bdd.726
Subject(s) - choroid plexus , bumetanide , chemistry , medicine , endocrinology , efflux , cerebrospinal fluid , lithium (medication) , ouabain , reabsorption , sodium , cotransporter , biochemistry , central nervous system , organic chemistry
The altered electrolyte handling of the choroid plexus was investigated in rats with acute renal failure (ARF) using lithium and rubidium as surrogate markers for sodium and potassium, respectively. Firstly, the transport of these two markers from the plasma to cerebrospinal fluid (CSF) was evaluated after they were concurrently injected into the femoral vein. As a result, their disposition from the plasma to CSF was shown to decrease in ARF rats, but the relationship profile between those two markers was not different from that observed in normal rats, indicating that the decreased disposition of lithium and rubidium occurs without affecting the stoichiometric balance. To clarify the mechanisms accounting for the decreased disposition, an inhibition study was then performed. When bumetanide, an inhibitor of the Na + /K + /2Cl − co‐transporter, was directly introduced into the cerebroventricle prior to lithium and rubidium being intravenously administered, a marked increase in the markers' disposition was observed. However, such an increased disposition did not occur when bumetanide was injected into the femoral vein. Other inhibitors, such as amiloride for the Na + /H + exchanger and ouabain for Na + /K + ‐ATPase, did not show any effects on marker disposition regardless of the inhibitor being administered into either the cerebroventricle or femoral vein. These findings suggest that the decreased marker disposition in ARF rats is due to an increased efflux process of the choroid plexus mediated by the Na + /K + /2Cl − co‐transporter. That is, electrolyte efflux from the CSF to plasma increases, and thereby the electrolyte influx from the plasma to CSF is counteracted. Copyright © 2010 John Wiley & Sons, Ltd.