Sodium Transport in the Choroid Plexus and Salt-Sensitive Hypertension

Abstract

To elucidate the role of epithelial sodium channels (ENaCs) and Na + -K + -ATPase in Na + transport by the choroid plexus, we studied ENaC expression and Na + transport in the choroid plexus. Lateral ventricle choroid plexuses were obtained from young male Wistar, Dahl salt–resistant (SS.BN13), and Dahl salt–sensitive (SS/MCW) rats on a regular (0.3%) or high- (8.0%) salt diet. The effects of ENaC blocker benzamil and Na + -K + -ATPase blocker ouabain on sodium transport were evaluated by measuring the amounts of retained 22 Na + and by evaluating intracellular [Na + ] with Sodium Green fluorescence. In Wistar rats, ENaC distribution was as follows: microvilli, 10% to 30%; cytoplasm, 60% to 80%; and basolateral membrane, 5% to 10%. Benzamil (10 −8 m ) decreased 22 Na + retention by 20% and ouabain (10 −3 m ) increased retention by 40%, whereas ouabain and benzamil combined caused no change. Similar changes were noted in intracellular [Na + ]. In Dahl rats on a regular salt diet, intracellular [Na + ] was similar, but the amount of retained 22 Na + was less in sensitive versus resistant rats. High salt did not affect ENaC mRNA or protein, nor the benzamil induced decreases in retained 22 Na + or intracellular [Na + ] in either strain. However, high salt increased intracellular [Na + ] and attenuated the increase in uptake of 22 Na + by ouabain in resistant but not sensitive rats, suggesting a decrease in Na + -K + -ATPase activity only in resistant rats. These findings suggest that both ENaC and Na + -K + -ATPase regulate Na + transport in the choroid plexus. Aberrant regulation of Na + transport and of Na + -K + -ATPase activity, but not of ENaCs, might contribute to the increase in cerebrospinal fluid [Na + ] in Dahl salt-sensitive rats on a high-salt diet.