Na(+)-H+ exchange in choroid plexus and CSF in acute metabolic acidosis or alkalosis.

Basolateral Na(+)-H+ exchange was analyzed with an in vivo model of choroid plexus (CP) epithelium in nephrectomized adult rats anesthetized with ketamine. Acid-base balance in blood was altered for 1 h over a pH continuum of 7.19 to 7.53 by equimolar intraperitoneal injections of HCl, NH4Cl, NaCl, or NaHCO3. Compartmental analysis enabled determination of CP intracellular pH (pHi) [dimethadione (DMO) method] and the choroid cellular concentration of 23Na (stable) and 22Na (tracer). HCl acidosis reduced the outwardly directed transmembrane basolateral H+ gradient, lowered the [23Na]i by 25%, and decreased the influx coefficient (Kin) for 22Na from blood into CP parenchyma (by 45% from 0.211 to 0.117 ml.g-1.h-1) and into cerebrospinal fluid (CSF) (by 43%, from 0.897 to 0.516). Compared with acid-loaded rats (HCl or NH4Cl), the NaHCO3-alkalotic animals had significantly enhanced uptake of 22Na into the CP-CSF system. This pH-dependent transport of Na+ from blood to CP was abolished by pretreatment with amiloride, an inhibitor of Na(+)-H+ exchange. Except in severe acidosis (HCl), the choroid cell pHi (7.05 +/- 0.02 in NaCl controls) and [HCO3-] (11-12 mM) remained stable in the face of acidemic and alkalemic challenges. With respect to reaction of the blood-CSF barrier to plasma acid-base perturbations, the responses of the fourth ventricle plexus pHi, [Na+]i, and 22Na uptake were similar to corresponding ones in lateral plexuses. We conclude that in the choroidal epithelium there is a Na(+)-H+ exchange activity capable of modulating Na+ flux into the CSF by approximately 50% as arterial pH is varied from 7.2 to 7.5.