The choroid plexuses are involved in cerebrospinal fluid (CSF) secreti
on and CSF K homeostasis. We examine K transport mechanisms present in
the isolated rat choroid plexus that may be involved in these functio
ns, predominantly using Rb-86 as a marker for K. The study demonstrate
s that there are two primary uptake mechanisms. Ouabain-sensitive Na-K
-adenosinetriphosphatase and bumetanide-sensitive cotransport, probabl
y of the Na-K-2Cl form, account for 48 and 46% of uptake, respectively
. Efflux studies demonstrate that the primary K efflux mechanism is al
so bumetanide-sensitive cotransport with the other major component pro
bably being by K channels as it is inhibitable by barium or quinidine.
Efflux via the cotransporter was not inhibited by R(+)-butylindazone,
a KCI cotransport inhibitor, but it was enhanced in the presence of o
uabain (P < 0.001) or increased extracellular Na concentration (P < 0.
01). Furthermore, Na efflux was bumetanide sensitive (P < 0.05). in al
l, these data suggest that the efflux cotransporter is also of the Na-
K-Cl form and that it is the same transporter as the influx mechanism
operating in both directions. The evidence presented leads us to hypot
hesize that this cotransporter is on the apical membrane of the choroi
d plexus and that it may have a central role in CSF secretion and perh
aps CSF K homeostasis.