The effect of lithium on electrolyte transport by the in situ choroid plexus of the cat.

Abstract

SUMMARY1. The effects of lithium on electrolyte transport were studied by using the cat choroid plexus isolated in a chamber in situ.2. Lithium infused intravenously to produce plasma lithium concentrations up to 5 m-equiv/l. caused an increase in plasma magnesium with no effect on the concentration of magnesium in the chamber fluid.3. When 22NaCl was infused intravenously the chamber fluid/plasma ratio of 22Na was nearly 1 in the first 30 min sample and at the steady state it was significantly greater than 1.4. When lithium chloride (1-5 m-equiv/l.) or potassium chloride (6.6 m-equiv/l.) was added to the chamber at the start of a collection period with plasma 22Na in the steady state, the 22Na content of the chamber fluid promptly increased 118 and 68 %, respectively, above the control value with no increase in secretary rate.5. The addition of ouabain to the chamber fluid, in addition to the lithium chloride or potassium chloride, tended to stimulate or have no significant effect on 22Na uptake at a concentration of 10-5 M and to reduce it as well as the secretary rate at 10-3 M.6. The data are compatible with there being two functionally separate sodium transport systems in the choroid plexus. One transports sodium accompanied by an anion and water to provide the fluid secreted into the chamber (c.s.f.) and the other operates primarily to regulate the potassium concentration of the c.s.f. by pumping potassium out in exchange for sodium.7. Lithium can be transported by both systems to a limited extent and the presence of lithium in the c.s.f. stimulates the sodium-potassium regulating pump.

Kinetics of the sodium pump in the frog choroid plexus.

“…The lack of effect of Li+ on sodium efflux (Fig. 3) is inconsistent with observations of Reed & Yen (1980) on the effect of 22Na transport across a cat choroid plexus preparation. They found that Li+ increased the 22Na content of fluid bathing the choroid plexus.…”

Molecular Modeling of Cerebrospinal Fluid Dynamics in Pediatric Pseudotumor Cerebri Syndrome: Altered Sodium Transport in Choroid Plexus by Lithium Treatment

“…Therefore, the results from investigations of different species consistently found that Li in CSF stimulated plasma Na (and presumably water) turnover into the ventricles. 43 Overall, these findings of increased Na transport by choroid plexus, and the putatively excessive CSF formation in a state of Li loading, suggest that the Na-transport inhibitors (e.g., amiloride, acetazolamide-congeners, and spironolactone) deserve further consideration as therapeutic agents to reduce the elevated ICP of PTCS in children and adults. [1][2][3][4][5][6] Fluid-Transport Modeling of Pseudotumor Cerebri Syndrome: Proposed Future Opportunities Assessing plasma Na flux into central nervous system is key to understanding PTCS pathophysiology and pharmacologic remediation.…”

The role of brain barriers in the neurokinetics and pharmacodynamics of lithium

“…Similarly to BBB, Na related transporters/channels might be also involved in the Li transport across the BCSFB [94,95] (Figure 2). NHE1 is not expressed in the human choroid plexuses, while it is still unknown whether the other NHE isoforms (such as NHE5) are expressed or not [96][97][98][99].…”